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    12-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Adrenal gland problems in CFS - why they occur - Dr. Buttar's Blog
    Klik op de afbeelding om de link te volgen













     

















        Adrenal gland problems in CFS

                        - why they occur -
                        Dr. Buttar's Blog

    Dr. Buttar's Blogmaster, September 22nd, 2008

    I see chronic fatigue syndrome as a stress induced disorder, by which I mean infectious stress, physical stress, mental stress, emotional stress and so on.
    The body deals with stress in ways which are either specific to that particular stressor (such as immune activation with a virus) or a general response to stress.
    As a part of that general response to stress, the adrenal glands are centrally important.
    This was well illustrated in some work done after the Second World war by the German physiologist Hans Selye.

    Selye stressed rats in nasty ways (which you and I do not want to think about).
    If he sacrificed these stressed rats he found that the adrenal gland had got larger.
    This was in order to allow it to produce more of the stress hormones cortisol, DHEA and probably others as well.

    If Selye took some rats and stressed them and then gave them a rest, he found that the adrenal glands had returned back to their normal size.

    In a third experiment Selye took rats and stressed them unremittingly with no break or rest.
    Initially the rats appeared to function fairly normally.
    However they suddenly became ill and died and when he examined them, he found that the adrenal gland had wasted away.

    I suspect this is what is happening in many of my chronic fatigue syndrome patients.
    I liken the adrenal gland to the gearbox in a car.
    When the stress goes on one can move up into third or fourth gear or even into overdrive to cope with that stress.
    However, one then needs a time of rest and recuperation for the body to recover.
    This system is necessary because if we all went round in overdrive all the time, we simply would not be able to fuel all of that activity and we would die from starvation.
    The body has to able to adjust its level of arousal to cope with the stresses of life.

    In evolutionary terms we are evolving faster now than at any previous stage and this involves us having to make changes to our lifestyle.
    Changes, whether that be change in relationships, moving house, changing jobs or whatever are inevitably stressful events.
    That combined with the fact that the population of the world is increasing and therefore we have more viruses which spread rapidly round the world causing infection, combined with the fact that the quality of our food is declining and we are further contaminating ourselves with toxic chemicals, means that our stress levels have never been greater.

    Different people can tolerate different amounts of stress.
    However, we all have our limits and anyone who is sufficiently stressed will eventually develop a “burnout syndrome”.
    This is what happens when the adrenal gland fails. Coming back to the analogy of the car, this means that when the stress goes on we can no longer move into fourth or fifth gear to cope with the stress, we can only struggle on in first.
    This manifests in the body clinically with severe fatigue, both physical and mental, sleep disturbance and many other physical symptoms, which of course are all the symptoms of a chronic fatigue syndrome.

    In order to allow the adrenal glands to recover, one needs a long time of reducing mental and emotional stress, excellent diet, good nutrition and reduction of toxic stress in order to allow the adrenal gland to recover.
    It does, but it takes time.

    Cfr. : http://www.drbuttar.com/blog/2008/09/adrenal-gland-problems-in-cfs-why-they-occur/



     Underactive Adrenal Gland
    - Stresses and Problems with the Body's 'Gear Box' -

    Dr. Sarah Myhill, MD
    March 10, 2009

    Dr. Sarah Myhill is an internationally recognized UK-based fatigue specialist focused on nutrition and preventive medicine, who sees ME/CFS as a stressor-induced disorder.
    Comparing the body to a car, she describes the cells' energy-producing mitochondria as the engine, thyroid as the accelerator pedal, and the adrenal system as the gear box.

    Dr. Sarah Myhill, MD, is a UK-based fatigue specialist focused on nutrition and preventive medicine.
    This information is reproduced with kind permission (article 443, January 2009) from her educational website – cfr. :
    http://www.drmyhill.co.uk/ -.
    For ME/CFS patients, a special feature of Dr. Myhill's site is her free 179-page online book - "Diagnosing and Treating Chronic Fatigue Syndrome" (cfr. :
    http://www.drmyhill.co.uk/cfs_book.pdf -).

    Cfr. also Dr. Myhill’s recent article with Drs. John McLaren-Howard and Norman Booth - “Chronic Fatigue Syndrome and Mitochrondrial Dysfunction” (cfr. : http://www.prohealth.com//library/showArticle.cfm?libid=14274 -) introducing “a biochemical test which measures energy supply to body cells and therefore fatigue levels in people with Chronic Fatigues Syndrome/Myalgic Encephalomyelitis (CFS/ME)”.


    The adrenal gland is responsible for the body's hormonal response to stress

    The adrenal gland – cfr. : http://en.wikipedia.org/wiki/Adrenal_gland - produces adrenaline, which stimulates the instant stress hormone response (fight or flight reaction).
    It also produces cortisol and DHEA, which create the short- and long-term stress hormone responses :

    • Cortisol suppresses the immune system, breaks down tissues and has a generally catabolic effect [breakdown of large molecules into smaller ones to release energy].

    • However, these effects are balanced out by DHEA, which has the opposite effect - activating the immune system and building up tissues.

    All these hormones are made from cholesterol - just one reason why running a low cholesterol is not necessarily a good thing !
    Both cortisol and DHEA are essential for life - too little cortisol causes the life threatening Addison's disease (cfr. :
    http://www.endocrine.niddk.nih.gov/pubs/addison/addison.htm -); too much causes the debilitating condition Cushing's syndrome (cfr. : http://www.endocrine.niddk.nih.gov/pubs/cushings/cushings.htm -).


    The name of the game is to get the right balance

    To achieve this, both hormones must be measured.
    This can be done with the Adrenal Stress Index (ASI) test.
    By measuring and supplementing within the physiological [up to and not exceeding normal] range, with biologically identical hormones, one is not going to get any unpleasant side effects; i.e., we are trying to copy Nature and restore normality.

    The ASI test looks at cortisol and DHEA levels over 24 hours.
    This test entails taking salivary samples through the day (yippee, no needles !).
    Indeed, salivary sampling is felt to be the most accurate way of assessing steroid hormone levels.

    An abnormal result may be a symptom of other problems or it may cause problems in its own right.
    The response of the body to stress (any stress - infectious, nutritional, emotional, physical etc) is to increase the output of stress hormones.
    This gears the body up for action by :

    • raising blood pressure,

    • increasing heart rate,

    • improving mental alertness (which can cause anxiety),

    • increasing energy supply and so on.

    It is actually metabolically very inefficient because it uses up lots of energy, but totally desirable if one has to fight for one's life !
    This reaction is essential for short term stress, but unsustainable long term.
    So time for rest and recovery is equally essential.


    Problems arise when the stress is unremitting, because eventually the output of the adrenal gland will reduce, making one far less able to tolerate stress

    Indeed this is often a complaint of my CFS patients - they simply do not tolerate stress at all well.
    The pattern of the result from the adrenal stress test gives some idea where one is along the stress response time line.

    A typical CFS adrenal stress profile test result showing low levels of cortisol and DHEA is depicted on page 83 of Dr. Myhill's free online book 'Diagnosing and treating chronic fatigue syndrome' (cfr. : http://www.drmyhill.co.uk/cfs_book.pdf -).


    Interpretation of The Adrenal Stress Index Test for DHEA and Cortisol Levels

    Levels of DHEA and cortisol vary according to the level of stress and for how long that stress has been applied. Increasing cortisol production is the normal response to stress and is highly desirable, so long as the stress is removed and the adrenal glands can recover.

    On-going, unremitting stress means the adrenal gland and the whole body is in a constant state of alert, does not get time to recover and eventually packs up.
    So, there are several stages of adrenal function gradually leading to failure :

    1. Normal levels of cortisol and normal DHEA.
      Normal result.
      Normal adrenal gland.

    2. Raised cortisol, normal DHEA.
      This indicates a normal short term response to stress.

    3. Raised cortisol and raised DHEA.
      The adrenal gland is functioning normally but the patient is chronically stressed.
      So long as the stress is removed, the adrenal gland will recover completely.

    4. High levels of cortisol, low levels of DHEA.
      The body cannot make enough DHEA to balance cortisol.
      This is the first sign of adrenal exhaustion.
      This is the first abnormal response to chronic stress.
      The patient needs a long break from whatever that chronic stress may be.
      The commonest chronic stress is hypoglycemia, but also consider insomnia, mental, physical or emotional overload or whatever.
      DHEA can be supplemented to make the patient feel better, but it must be part of a package of recovery without which worsening can be expected.

    5. Cortisol levels low, DHEA levels low.
      The gland is so exhausted it can't make cortisol or DHEA.
      By this time patients are usually severely fatigued.

    6. Cortisol levels low, DHEA borderline or normal.
      This probably represents the gland beginning to recover after a long rest.
      DHEA may be used to help patients feel better whilst they continue their program of rest and rehabilitation.


    In Addison's disease there is complete failure of the adrenal gland not because of chronic stress but because of autoimmunity

    This is a life threatening disorder and the patient is severely ill.
    The main clinical symptom is severe postural hypotension [aka POTS or dizziness when rising to an upright position, diagnosed via a Tilt Table Test] and chronic hypoglycemia.

    Addison's disease is tested for by a short synacthen test in which cortisol levels are measured before and after an adrenal gland stimulant ACTH [also known as the short or rapid ACTH test].
    Many patients with CFS are given this test, which is found to be normal resulting in the patient being told their adrenal gland is fine and no action is required.

    The problem with this test is it only shows where the adrenal gland is completely non-functioning - it does not diagnose partial adrenal failure or adrenal stress and no measurements of DHEA are made.
    This makes it potentially misleading.


    Treatment

    The idea with treatment with cortisol and with DHEA [supplementation] is to stay within physiological ranges - up to, but not more than, normal amounts.
    By doing this there are no side effects in the short or long term.
    Many doctors and patients recoil at the prospect of taking steroid hormones.
    Remember, all the side effects of steroid hormones are created by the dose.
    Using physiological as opposed to pharmacological doses avoids all these problems.

    A normal adrenal gland produces about 10-50mgs of DHEA daily and 20-25mgs of hydrocortisone daily.
    Steroid side effects would appear after a few weeks of 100mgs a day or a few months at 50mgs a day
    .

    DHEA is available over the counter in the U.S., where the FDA has classified it as a food supplement up to a daily dose of 25mgs....

    I start my patients on 12.5mgs (for small people) and 25mgs (for larger people) of DHEA a day, taken in the morning.
    I like to recheck a single DHEA after 3 months to make sure I am staying within physiological ranges and because a few patients need 50mg.

    Cortisol again needs to be used in sub-physiological doses – i.e., up to, but not more than 10mgs a day (please note that the usual steroid most often used is prednisolone; 5mgs of prednisolone is equivalent to 20mgs of hydrocortisone).
    Both these are prescription only drugs.

    After 3 to 6 months, if the patient wishes to continue taking DHEA, then levels need to be re-checked by doing a single sample salivary DHEA (you can order this test from my website - DHEA (saliva) single (cfr. 'DHEA (saliva) single - Lab 21' at : http://www.drmyhill.co.uk/test.cfm?id=23 -) - and elsewhere online for those outside the UK.

    Cortisol levels replete reliably well and it is not necessary to recheck cortisol levels.

    As the patient improves, usually hydrocortisone can be stopped - typically after 1 to 2 years.
    I suspect DHEA is an acquired metabolic dyslexia - that is to say, as we age we get less good at making it :

    • Young people can often stop DHEA as they improve and maintain levels,

    • But older people often benefit from taking DHEA long term.


    Low-Dose Hydrocortisone CFS Trial

    In a randomized, controlled, crossover trial of low-dose hydrocortisone treatment for CFS ('Low-dose hydrocortisone in chronic fatigue syndrome - A randomised crossover trial' - Dr. Anthony J Cleare, et al. Lancet; Vol 353, issue 9151 – cfr. : http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(98)04074-4/fulltext -), 32 participants, fulfilling both the Oxford and CDC 1994 criteria, completed this short-term trial.
    Participants received 5mg or 10mg of hydrocortisone for 28 days and placebo for 28 days.

    The results revealed modest, statistically significant improvements in fatigue with this low-dose hydrocortisone treatment compared with placebo.
    The degree of disability was also reduced with hydrocortisone treatment but not with placebo.
    There was no significant difference in changes in fatigue score when 5mg and 10mg doses were compared.

    The authors suggest that, in view of the lack of dose response in this study, 5mg is a sufficient low dose of hydrocortisone.

    Participants who responded to this hydrocortisone treatment did not differ from "non-responders" in terms of their pre-treatment cortisol levels.
    Although none of the participants in this study had a current psychiatric illness, those who responded to hydrocortisone treatment had fewer psychiatric symptoms prior to treatment.

    Based on the results of the insulin stress test, this short-term, low dose hydrocortisone treatment was not found to cause significant suppression of adrenal gland function.
    None of the participants dropped out of the study and only minor side effects were reported.

    The authors conclude that this low-dose hydrocortisone treatment resulted in "significant reduction in self-rated fatigue and disability in patients with chronic fatigue syndrome".


    Comment

    This study sheds interesting light on the possible role of low cortisol levels in the disease processes involved in CFS.
    Caution is required, however, in interpreting the results.
    Participants' baseline cortisol levels could not predict their response to hydrocortisone treatment and participants appeared to have baseline cortisol levels within the normal reference range.

    In another randomized controlled trial of low-dose hydrocortisone therapy in CFS – cfr. 'Low-Dose Hydrocortisone for Treatment of Chronic Fatigue Syndrome' at : http://jama.ama-assn.org/cgi/content/full/280/12/1061 -, McKenzie et al. used a higher "low-dose" hydrocortisone treatment of 25 to 35mg daily.
    They found that this dose was associated with some improvements in symptoms but caused significant adrenal suppression.

    Neither of these research teams currently recommended the use of hydrocortisone as a treatment for CFS.
    The Cleare study assessed the effects of hydrocortisone treatment in the short-term only.
    As the authors point out, further studies involving longer durations of treatment and follow-up [would be] required to assess the long-term effectiveness and safety of this treatment.

    Ed Note : Also on the high-profile subject of cortisol in ME/CFS, see "Recalibrating 'fight or flight' – counter-intuitive new treatment for chronic fatigue syndrome & other chronic stress disorders" – cfr. : http://www.prohealth.com//library/showArticle.cfm?libid=14271 - , summarizing a recent report by Drs. Ben-Zvi, Vernon and Broderick, suggesting a therapy that “challenges the conventional strategy of supplementing cortisol levels” for some patients.


    Cfr. : http://www.prohealth.com/ME-CFS/library/showArticle.cfm?libid=14383&B1=EM031109C


    12-03-2009 om 17:52 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 2/5 - (1 Stemmen)
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    11-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Tips for winning a fibromyalgia or chronic fatigue syndrome disability case... and... what actually happens at a social security disability hearing ?
    Klik op de afbeelding om de link te volgen


























     




































    Tips for winning
    a fibromyalgia or chronic fatigue syndrome
    disability case
    ...
    and...
    what actually happens
    at a social security disability hearing
    ?

    Jonathan Ginsberg, Attorney, Atlanta, Georgia - ProHealth, Inc., February 21, 2009

    Jonathan Ginsberg is a practicing Social Security attorney in Atlanta.
    This material is reproduced with kind permission of the author from his "Social Security Disability" resource website – cfr. :
    http://www.4socialsecuritydisability.net -.
    In addition to his website, Mr. Ginsberg maintains a blog – cfr. :
    http://www.ssdanswers.com -) where patients may submit questions and receive professional responses and an Internet Social Security Disability radio program featuring Q&A and interviews "about winning case strategies and forthcoming changes to the disability adjudication process."

    Jonathan Ginsberg is a Social Security Disability case lawyer specialized in representing patients with chronic illnesses such as Chronic Fatigue Syndrome and Fibromyalgia.
    He maintains a "Social Security Disability" website offering resources from disability lawyers all over the U.S., plus a blog and radio program where patients may submit questions and receive professional responses.
    Though he uses examples from FM cases here, the concepts apply equally to CFS and other "invisible" disabilities.


    1. - Tips for winning
    a fibromyalgia or chronic fatigue syndrome
    disability case

    In a disability case, you need to prove one thing - that you are not able to work.
    If you remember nothing else about Social Security disability, remember that your capacity for performing work is the only thing that matters to a Social Security judge.

    1.1 - Your ability to perform an easy job - the main issue

    Your underlying medical condition – FM, CFS or any other medical problem - is only important to the Social Security Judge if your symptoms limit you from performing a job 8 hours a day, 5 days a week.

    Thus, for example :

    • I have won cases in the Atlanta hearing offices in which my client’s medical problem was a moderate, functional heart defect, but in this client’s case, her anxiety about her condition was so severe that she could not concentrate at work.

    • Similarly, I have seen judges deny cases in which a claimant had three herniated discs, but was able to function in a minimally demanding job because of an unusually high pain threshold.

    In most cases, the judge’s decision really boils down to his/her decision about whether you could hold down a simple, sit-down type of job that requires no training; that allows you to sit, stand and adjust your position; and that is not production oriented.

    In fact, in most hearings, the Judge will call a ‘vocational expert’ to testify about work you have done in the past and about simple, minimally demanding jobs that exist in the national economy (cfr. the detailed description of "What Actually Happens at Your Social Security Disability Hearing" in the accompanying article, below].

    1.2 - Comprehensive medical records - A key to winning

    As a claimant’s lawyer, my job is to identify medical records that suggest work limitations.
    In many cases this means I need to review all of the medical records, then create a functional capacity checklist that includes both the limitations associated with your particular case and the impairment categories used in Social Security cases.

    We then ask your doctor to complete the checklist for submission to the Judge.

    Note that :

    • We do not ask the doctor to decide if you are ‘disabled’ - that is a legal decision for the Judge.

    • Instead, we ask your doctor to help ‘translate’ his medical conclusions into specific work limitations.

    1.3 - What is the Judge thinking ?

    There is a perception that Social Security disability cases based on Fibromyalgia [or Chronic Fatigue Syndrome] are difficult to win.
    It is true that some judges have a problem acknowledging a medical syndrome (not a "disease") that cannot be detected by a blood test and that can have a wide range of symptoms (cfr. the clinical definition of Fibromyalgia as set forth by the American College of Rheumatology at :
    http://www.nfra.net/Diagnost.htm – and the diagnostic driteria for Chronic Fatigue Syndrome at : http://www.immunesupport.com/chronic-fatigue-syndrome-diagnostic.htm -).

    Nevertheless, my experience has been that you can get creative in offering a Judge a theory of disability.

    Not too long ago, for example :

    • I represented a Fibromyalgia client before a Judge who called a psychiatrist as an expert witness.
      The Judge granted benefits on the ground that my client’s "fibro fog" was equivalent to a chronic state of anxiety - a psychiatric condition.

    • Two weeks later, I tried a different Fibromyalgia case before another Judge in the same hearing office.
      This Judge awarded benefits (correctly in my opinion) on the basis of a combined impairment - recognizing the combined effect of Fibromyalgia’s impact on my client’s physical and mental condition.

    • Yet a third Judge in this same hearing office granted another case on the basis that my client’s condition was equivalent to an orthopedic condition - severe arthritis.

    Obviously, I am most interested in winning cases for my clients, although I do find it interesting that some judges must really struggle to find a legal basis to award benefits.
    Further, I think it is fair to say that judges in big cities like Atlanta are probably more likely to see Fibromyalgia [and Chronic Fatigue Syndrome] patients supported by knowledgeable physicians and long treatment histories.

    Fortunately, even if judges don’t understand the condition, many will honor the opinion of your treating physician, especially if you have a long and continuous treatment record (the legal term for a thorough medical history is a "longitudinal treatment record").

    1.4 - Focus on specific symptoms

    I find that it is important to focus on Fibromyalgia symptoms other than just generalized body pain.
    Remember, judges see claimants every day complaining of "pain all over".
    These cases are not Fibromyalgia, but pains caused by arthritis, obesity, poor nutrition, mild diabetes etc.

    Judges are people and they tend to discount complaints they hear again and again.
    As you may know, Fibromyalgia or CFS often produce a number of other identifiable symptoms, including loss of balance, digestive problems, irritable bowel syndrome, slurred speech, vision problems, depression, swelling, memory loss, cognitive loss, fatigue, sleeplessness etc.

    Many patients get used to living with these symptoms and fail to mention all of them to their doctors or to the judge.

    One technique I recommend to my clients is to obtain a calendar and keep diary notes about how you feel and what symptoms you experience each day.
    Make lists.
    Ask for your spouse’s or children’s observations.
    It has been my experience that judges may not want to grant your case based on overall body pain, but may feel more comfortable focusing on your digestive or balance problems.
    Make the judge’s (and your lawyer’s) job easy !

    You might find it helpful to read a Judge’s decision in a Fibromyalgia case (the file at : http://www.4socialsecuritydisability.com/Fibro%20decision.pdf - offers two of my recent favorable Fibromyalgia decisions from the Atlanta Office of Hearings & Appeals).
    The first case involved a 38-year-old woman with an extensive job background who suffers from Fibromyalgia as well as numerous gastrointestinal and other complications.
    Note that the Judge focuses on my client’s work history and that she is very credible because she has been seeking a medical solution to her problem.

    1.5 - Deciding on a start-date for your disability

    I also have found that many of my Fibromyalgia clients were ambitious and hardworking in their careers and jobs.
    Subconsciously or otherwise, many Judges realize that few claimants would trade the money and job satisfaction of a challenging career for the fixed income offered by Social Security disability.

    I therefore usually encourage my clients to testify about :

    • what they did before they stopped work,

    • how they tried to hang on, even while fighting increasing levels of pain and fatigue and

    • how they would greatly prefer their former way of life.

    You may also be able to "push back" the starting date for your benefit payments if your last few weeks or months of work were not in the nature of "competitive employment".
    For example, if your boss allowed extra absences or changed your job description, the judge may find that you did not engage in competitive work activity.

    Similarly, if you previously applied for benefits, received a denial, then tried unsuccessfully to return to work, you may be eligible for months or years of past due benefits.
    Issues related to amending your onset date are beyond the scope of this article, but should be evaluated.

    Note : The comments and opinions expressed here should not be considered legal advice, as every Social Security Disability case is different and depends on your individual case information.
    Further, the author makes no warranty, express or implied, about the accuracy or reliability of this information.
    You should not act or rely on any information without seeking the advice of an attorney or qualified non-attorney representative.



    2. - 
    What Actually Happens
    at a Social Security Disability Hearing
     ?

    You have waited a year or longer.
    The big day is finally here.
    Your Social Security hearing is tomorrow.
    What is going to happen ?
    Who will be there ?
    What does the Courtroom look like ?
    Will you be asked a lot of questions ?

    Your hearing is your best chance for winning disability benefits.
    Prior to the hearing, your case was evaluated by a State Agency Adjudicator - a government employee whom you did not meet face to face and whose evaluation of your case was based on your medical records only.
    And, since your doctor’s reports did not contain certain medical terms, nor did they discuss specific vocational restrictions, your case was denied.
    For more information about the initial application and the reconsideration stage of your case, read this :

    How to Appeal your Denied Social Security Disability Case
    When you apply for disability benefits, there is a good chance that your application will be denied.
    Frequently deserving cases will be denied because the Social Security claims agent does not have medical records or other documentation to fully evaluate your claim.
    If you are denied, do not give up.
    You can and should appeal your denial by filing a "request for reconsideration" within 60 days after receiving your denial.
    If your reconsideration appeal is also denied, you can and should request a hearing before a Social Security judge.
    Here, too, you have 60 days to file an appeal.
    You may wish to consult useful publications for assistance in completing Social Security's forms.
    Attorney Jonathan Ginsberg's Disability Answer Guide ('Social Security disability forms' – cfr. :
    http://www.disabilityforms.com/ -) as well as the Nolo Guides are examples of written and recorded products that can help you make sense of the confusing appeals process and can significantly improve your chances at winning early.
    When you request a Social Security hearing, your case will be assigned to an administrative law judge in your community.
    Unlike the Social Security claims agents, Social Security judges have much more decision making power to approve your case.
    In most cases, you are better off retaining a lawyer to represent you in a hearing before a judge.
    Social Security lawyers will typically handle your case under a contingency fee contract, meaning that there is no fee unless you win.
    Often you can expect to pay your lawyer 25% of past due benefits collected.
    When you choose a lawyer, you will enter into an attorney-client fee agreement that spells out the terms any fees that are charged.
    If you lose at your hearing, there are two more levels of appeal - the Appeals Council and Federal District Court.
    Both of these appeals should be undertaken with the assistance of an experienced lawyer.
    Cfr. :
    http://www.4socialsecuritydisability.com/Appeal_process.htm -.

    At a hearing, you will have the opportunity to tell your story to an experienced Administrative Law Judge.
    Your Judge is not bound by any of the findings made by the State Agency Adjudicator.
    In other words, the Judge will look at your case with a fresh pair of eyes and he or she will have the chance to meet you and look you over.

    While it is normal for you to be nervous, you should realize that most Judges want to make a fair decision and that you will be treated with dignity and respect.
    It is important, however, to know what to expect.

    2.1 - What does the Hearing Room look like ?

    The hearing room in a Social Security case is much different than traditional courtrooms you may have seen live or on TV :

    • your hearing room will be small and informal

    • the hearing will be held around a conference table

    • you will also notice an audio tape recorder and microphones used to tape the hearing

    • unlike regular court cases, Social Security hearings are not open to the public - therefore, there are no seats for spectators

    • most people like the small, informal setting; this type of set-up should help you relax and establish a dialog with the judge.

    2.2 - Who will be there ?

    The participants at a hearing will be the Judge, a hearing assistant (who operates the tape machine), you, your lawyer and possible one or more expert witnesses.

    2.2.1 - Why will expert witnesses be present at my hearing ?

    • Social Security Judges use expert witnesses to help them better understand the issues in your case

    • Expert witnesses are not there to hurt you or to help you

    • Expert witnesses come from a panel of experts selected by Social Security

    • When the Judge decides to call an expert witness, he cannot ask for a particular witness - instead, a member of the panel is assigned randomly.

    2.2.2 - The Vocational Expert
    In most cases, the Judge will call a "Vocational Expert" (also called a 'VE').

    • The VE may be a job placement professional, a professor or a vocational rehab counselor.

    • The VE’s job is to classify your past work and describe for the judge the skill level of your past work (unskilled, semi-skilled or skilled) along with the exertional level called for in this job (sedentary/sit-down, light, medium or heavy).

    • The judge needs this information to determine whether your claimed impairment would prevent you from returning to your past work and whether you have acquired any skills that would transfer to less demanding work.

    • Vocational experts will be familiar with a publication called the Directory of Occupational Titles - which is a book published by the U.S. Department of Labor that describes the physical and mental requirements of all jobs that exist in the United States.

    2.2.3 - Examples of Vocational Expert testimony
    The Judge will use the VE to "translate" your medical problems into work limitations.
    After listening to your testimony, the Judge will turn to the Vocational Expert and pose one or more questions about your job capacity.
    For example, in a recent hearing the Judge posed the following questions to the VE :

    • "Mr. VE, assume I find that the claimant is 48 years old, with a high school education and has past work as a machine operator, as a shift supervisor at a convenience store and as a shift supervisor at a retail store.
      Further assume that I find that the claimant has been diagnosed with fibromyalgia and has a moderate level of pain all the time.
      Further assume that the claimant can stand for no more than 20 minutes at a time and that standing can constitute no more than 2 hours total during a work day.
      Sitting is unlimited, although the claimant needs a "sit/stand" option.
      Could this claimant return to her past work ?
      Could she do any other work ?

    • "Mr. VE, assume the same limitations set out in question 1, but add the following limitations.
      Assume that I find that the claimant’s testimony is credible in her statement that her pain level rises to a "severe" level at least one hour per day at unpredictable times.
      This severe level of pain would cause a significant interference with attention and concentration.
      Assume further that as a result of pain, the claimant would likely leave work early or miss work entirely 1 to 2 days per week.

    What does all this mean ?
    In response to question Number 1, the VE testified that the claimant could not return to past work, but could perform a variety of unskilled, sedentary jobs.

    In response to question Number 2, the VE testified that the claimant could not return to either past work or to any other job.
    The point of this is to show you how the wording of the question to the VE can result in a win or a loss.
    That is why it is so important to get your doctor’s cooperation in identifying specific work activity limitations arising from your medical condition.
    Further, your testimony should be both truthful and consistent with the limitations set out by your doctor.
    As your attorney, our job is to explain to you what is in your file and practice your testimony.

    2.2.4 -The Medical Expert
    In some cases, your Judge will call a Medical Expert as well as a Vocational Expert.
    In our experience, a Judge will call a Medical Expert :

    • If your medical record is long and complicated;

    • If you have been diagnosed with multiple conditions;

    • If there is contradictory information in your medical record.

    Some Judges call Medical Experts (also called ME’s) frequently.
    Other judges call them rarely.
    Currently, the ME panel includes psychiatrists, psychologists, orthopedists, internists, cardiologists and other specialists.
    It has been our experience that the quality of testimony from various medical experts varies widely.
    Some Medical Experts testify frequently and understand the underlying vocational nature of a Social Security case.
    Other ME’s provide very little help.
    Your attorney is permitted to cross examine the ME, either to clarify a point or to discredit the testimony if it is out of line.
    Vocational Expert testimony, by contrast, is usually much more consistent and predictable than Medical Expert testimony.

    2.2.5 - Where do you sit and who says what ?
    When you enter the hearing room, you will be directed to sit in a specific chair, usually one that is facing the Judge.
    The Judge will introduce himself/herself along with the Hearing Assistant and the Vocational and/or Medical Expert witnesses.
    He will then ask your attorney to state his/her name.
    The Judge will then read a very brief statement setting out the issues to be heard.
    In most cases, he will ask your lawyer to waive a formal reading of the issue.
    The Judge will then ask your lawyer if he/she has any objections to exhibits in the record and if there are any outstanding records not in your file.
    One of the things you should expect from your lawyer is a diligent effort to obtain up-to-date copies of your medical records.
    Remember, the Hearing Office will not update your records - this is your responsibility.
    It has been our experience that your Judge will be upset (and may even postpone the hearing) if important medical reports are missing.
    For this reason, you should contact your lawyer’s office regularly to advise them of new treatment, new doctors etc.
    Assuming no objections, the Judge will swear you in to tell the truth.
    If your religious beliefs do not permit you to take a sworn oath, you may affirm that your statements will be true.
    The Judge may then ask your lawyer for an Opening Statement.
    Again, some Judges do and others do not.

    2.2.6 - Your testimony
    Every Judge has a different technique with regard to questions and testimony.
    Most Judges will ask all the questions, offering your lawyer a chance to follow up.
    Other Judges leave all questioning to your lawyer.
    The subjects covered in your direct examination include :

    • background information - your age, education, marital status, living arrangements (home, apartment etc.)

    • discussion of past work as performed - lifting, carrying, supervisory roles etc.

    • specific discussion of medical problems and activity limitations.

    What you must remember when testifying
    The most important things for you to remember when testifying are as follows :

    • Tell the truth

    • Be specific - instead of saying : "I can’t walk very far and I can’t lift very much," say : "It’s about 25 yards to my mailbox. When I get to the mailbox, I have to stop because my knees hurt so bad and my chest hurts. When I come back, I have to support myself on a fence so I won’t lose my balance"
      "As far as lifting, I tried to lift a gallon of milk about a month ago, but I could not hold it, even with both hands and it fell and spilled all over the floor."

    • It is very important that you remember and practice being specific.
      It has been our experience that you will be nervous and that at a hearing, it will be hard to think about how much you can lift, how far you can walk etc.
      Practice ahead of time !

    • Be very descriptive when describing pain.
      Don’t say : "It hurts a lot";
      Instead, say : "when I get a migraine, I can’t do anything. I feel nauseated and sick. I turn off the lights, lie in bed with a cold compress on my forehead and try not to think at all. It usually takes my medicine about an hour to kick in - even that does not help - it just puts me to sleep."

    • If you need to stand up and walk around, do so.
      Judges don’t mind if you have to stretch out.
      This is especially important if you testify that you can sit without interruption for no more than 15 minutes, then sit still at your hearing for an hour.

    • Say : "yes" or "no"m not "uh-huh" or "huh ?" or just nod or shake your head.
      Remember that your hearing is being tape recorded.

    • Don’t curse.

    • Dress neatly - you don’t need your Sunday best, but you should avoid blue jeans and T-shirts.

    • Bring your bottles of medicine - the Judge may want to see them.

    • Your attitude during your testimony is important.
      Remember that your Judge sees claimants every day who want benefits.
      Your attitude ought to be : "if I could work I would work".
      Describe for the Judge what you did and how you enjoyed being productive and useful.

    • Don’t tell the Judge that you are "disabled" - that is his job to decide.
      After listening to your testimony, the Judge will then take the Expert Witness testimony and ask questions of the Expert Witnesses.
      Your attorney will also be given an opportunity to ask questions of the Expert Witnesses.

    Finally, the Judge may ask you if you have any final comments.
    If everything was covered in your testimony, its OK to say "no."
    Respect the fact that the Judge has other hearings and time constraints.
    In most cases, the Judge will not issue a decision at the end of the hearing.
    You can expect to receive a written decision in four to six weeks, sometimes longer.

    Note : The comments and opinions expressed here should not be considered legal advice, as every Social Security Disability case is different and depends on your individual case information.
    Further, the author makes no warranty, express or implied, about the accuracy or reliability of this information.
    You should not act or rely on any information without seeking the advice of an attorney or qualified non-attorney representative.

    Cfr. : http://www.prohealth.com/ME-CFS/library/showArticle.cfm?libid=12585&B1=EM031109C


    11-03-2009 om 22:59 geschreven door Jules

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    10-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.CFS Myths - Part I
    Klik op de afbeelding om de link te volgen


    CFS Myths
    Part I

    International Association for CFS/ME (IACFS/ME)

    The question with CFS or any illness is : counting all of the published reports and the numbers of patients in all of these reports, do the great majority of reports involving the great majority of patients find objective biological abnormalities ?
    The answer for CFS, with regard to studies of the nervous system and immune system, is yes.

    Myth 1 - CFS is a disease defined just by a group of symptoms. There are no objective abnormalities

    Many published studies report abnormalities of the central nervous system, autonomic nervous system and immune system in patients with CFS-abnormalities not present in comparison groups who are healthy or have other fatiguing illnesses.

    • The importance of orthostatic intolerance in the chronic fatigue syndrome
      Schondorf R, Freeman R, Dept. of Neurology, McGill University, Sir Mortimer B. Davis Jewish General Hospital, Montreal, Quebec, Canada : cxrs@musica.mcgill.ca - Am J Med Sci. 1999 Feb;317(2):117-23 - PMID: 10037115
      Chronic fatigue syndrome (CFS) or myalgic encephalomyelitis is a clinically defined syndrome characterized by persistent or relapsing debilitating fatigue for longer than 6 months in the absence of any definable medical diagnosis.
      The cause of this syndrome is unknown.
      Symptoms of orthostatic intolerance, such as disabling fatigue, dizziness, diminished concentration, tremulousness and nausea, are often found in patients with CFS.
      In this review, we critically evaluate the relationship between orthostatic intolerance and CFS.
      Particular emphasis is placed on clinical diagnosis, laboratory testing, pathophysiology and therapeutic management.
      It is hoped that this review will provide a stimulus for further study of this complex and disabling condition.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/10037115

    • Blunted adrenocorticotropin and cortisol responses to corticotropin-releasing hormone stimulation in chronic fatigue syndrome
      Scott LV, Medbak S, Dinan TG, Department of Psychological Medicine, St Bartholomew's and the Royal London School of Medicine, West Smithfield, UK - Acta Psychiatr Scand. 1998 Jun;97(6):450-7 - PMID: 9669518
      Hypofunctioning of the pituitary-adrenal axis has been suggested as the pathophysiological basis for chronic fatigue syndrome (CFS).
      Blunted adrenocorticotropin (ACTH) responses but normal cortisol responses to exogenous corticotropin-releasing hormone (CRH), the main regulator of this axis, have been previously demonstrated in CFS patients, some of whom had a comorbid psychiatric disorder.
      We wished to re-examine CRH activation of this axis in CFS patients free from concurrent psychiatric illness.
      A sample of 14 patients with CDC-diagnosed CFS were compared with 14 healthy volunteers.
      ACTH and cortisol responses were measured following the administration of 100 microg ovine CRH.
      Basal ACTH and cortisol values did not differ between the two groups.
      The release of ACTH was significantly attenuated in the CFS group (P < 0.005), as was the release of cortisol (P < 0.05).
      The blunted response of ACTH to exogenous CRH stimulation may be due to an abnormality in CRH levels with a resultant alteration in pituitary CRH receptor sensitivity or it may reflect a dysregulation of vasopressin or other factors involved in HPA regulation.
      A diminished output of neurotrophic ACTH, causing a reduced adrenocortical secretory reserve, inadequately compensated for by adrenoceptor upregulation, may explain the reduced cortisol production demonstrated in this study.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/9669518?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDoc
      Sum

    • Interindividual Immune Status Variation Patterns in Patients with Chronic Fatigue Syndrome - Association with Gender and the Tumor Necrosis Factor System
      Roberto Patarca MD, PhD, Department of Medicine, University of Miami School of Medicine, Miami, FL, 33101 - Nancy Klimas MD, Veterans Administration Medical Center, Miami, FL - Dmitry Sandler, Department of Medicine, University of Miami School of Medicine, Miami, FL, 33101 - Maria N. Garcia PhD, Department of Medicine, University of Miami School of Medicine, Miami, FL, 33101 - Mary Ann Fletcher MD, Department of Medicine, University of Miami School of Medicine, Miami, FL, 33101 - Journal of Chronic Fatigue Syndrome - Multidisciplinary Innovations in Research, Theory and Clinical Practice, Volume : 2 Issue : 1 : Pub Date : 04/15/1996 – ISSN : 1057-3321 - © Haworth Press, Inc. 2006
      Changes in soluble immune mediator levels in association with the chronic fatigue syndrome (CFS) usually occur within normal ranges and are apparent mainly as changes in the skewness of population distributions.
      The latter finding undermines the usefulness of cytokine levels as clinical tools at the individual level as has been seen in sepsis syndrome where a similar overlap occurs.
      Nonetheless, changes in cytokine levels at the population level can contribute to an understanding of the disease process.
      For example, we reported previously that significant proportions of CFS patients showed elevated serum levels of either soluble tumor necrosis factor-receptor I (sTNF-RI, sCD120a) or TNF-a as compared to controls.
      The latter results could reflect different disease processes or extremes of a common disease process.
      Using sera collected over a five-year period, we have now studied an extended cohort of 108 CFS patients and our results are consistent with a common graded disease process.
      When we assessed the effect of gender on the distributions of serum levels of immune mediators, levels of sTNF-RI, sTNF-RII (sCD 12Ob), sIL-6R (sCDl26, and sICAM-1 were found to be consistently higher among males than females and among CFS patients as compared to controls regardless of gender.
      Moreover, differences in soluble immune mediator levels between CFS and control individuals were more clearly defined when restricting the analysis to the female gender.
      These observations are consistent with endocrine influences on immunological changes.
      Cfr. :
      http://www.haworthpress.com/store/ArticleAbstract.asp?ID=78387

    • Interleukin-1 beta, interleukin-1 receptor antagonist and soluble interleukin-1 receptor type II secretion in chronic fatigue syndrome
      Cannon JG, Angel JB, Abad LW, Vannier E, Mileno MD, Fagioli L, Wolff SM, Komaroff AL, Department of Medicine, Tufts University-New England Medical Center, Boston, Massachusetts 02111, USA - J Clin Immunol. 1997 May;17(3):253-61 - PMID: 9168406
      Chronic fatigue syndrome is a condition that affects women in disproportionate numbers and that is often exacerbated in the premenstrual period and following physical exertion.
      The signs and symptoms, which include fatigue, myalgia and low-grade fever, are similar to those experienced by patients infused with cytokines such as interleukin-1.
      The present study was carried out to test the hypotheses that (1) cellular secretion of interleukin-1 beta (IL-1 beta), interleukin-1 receptor antagonist (IL-1Ra) and soluble interleukin-1 receptor type II (IL-1sRII) is abnormal in female CFS patients compared to age- and activity-matched controls; (2) that these abnormalities may be evident only at certain times in the menstrual cycle; and (3) that physical exertion (stepping up and down on a platform for 15 min) may accentuate differences between these groups.
      Isolated peripheral blood mononuclear cells from healthy women, but not CFS patients, exhibited significant menstrual cycle-related differences in IL-1 beta secretion that were related to estradiol and progesterone levels (R2 = 0.65, P < 0.01).
      IL-1Ra secretion for CFS patients was twofold higher than controls during the follicular phase (P = 0.023), but luteal-phase levels were similar between groups.
      In both phases of the menstrual cycle, IL-1sRII release was significantly higher for CFS patients compared to controls (P = 0.002).
      The only changes that might be attributable to exertion occurred in the control subjects during the follicular phase, who exhibited an increase in IL-1 beta secretion 48 hr after the stress (P = 0.020).
      These results suggest that an abnormality exists in IL-1 beta secretion in CFS patients that may be related to altered sensitivity to estradiol and progesterone.
      Furthermore, the increased release of IL-1Ra and sIL-1RII by cells from CFS patients is consistent with the hypothesis that CFS is associated with chronic, low-level activation of the immune system.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    • A 37 kDa 2-5A binding protein as a potential biochemical marker for chronic fatigue syndrome
      K De Meirleir, C Bisbal, I Campine, P De Becker, T Salehzada, E Demettre, B Lebleu - Am J Med. 2000 Feb ;108 (2):99-105 11126321
      Purpose
      - Recent studies have revealed abnormalities in the ribonuclease L pathway in peripheral blood mononuclear cells of patients with the chronic fatigue syndrome.
      We conducted a blinded study to detect possible differences in the distribution of 2-5A binding proteins in the cells of patients with chronic fatigue syndrome and controls.
      Patients and methods - We studied 57 patients with chronic fatigue syndrome and 53 control subjects (28 healthy subjects and 25 patients with depression or fibromyalgia).
      A radioactive probe was used to label 2-5A binding proteins in unfractionated peripheral blood mononuclear cell extracts and to compare their distribution in the three groups.
      Results - A 37 kDa 2-5A binding polypeptide was found in 50 (88%) of the 57 patients with chronic fatigue syndrome compared with 15 (28%) of the 53 controls (P < 0.01).
      When present, the amount of 37 kDa protein was very low in the control groups.
      When expressed as the ratio of the 37 kDa protein to the 80 kDa protein, 41 (72%) of the 57 patients with chronic fatigue syndrome had a ratio > 0.05, compared with 3 (11%) of the 28 healthy subjects and none of the patients with fibromyalgia or depression.
      Conclusion - The presence of a 37 kDa 2-5A binding protein in extracts of peripheral blood mononuclear cells may distinguish patients with chronic fatigue syndrome from healthy subjects and those suffering from other diseases.
      Cfr. :
      http://lib.bioinfo.pl/pmid:11126321

    • Spinal fluid abnormalities in patients with chronic fatigue syndrome
      Natelson BH, Weaver SA, Tseng CL, Ottenweller JE, CFS Cooperative Research Center and Department of Neurosciences, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, New Jersey, USA : bhn@njneuromed.org - Clin Diagn Lab Immunol. 2005 Jan;12(1):52-5 - PMID: 15642984
      Arguments exist as to the cause of chronic fatigue syndrome (CFS).
      Some think that it is an example of symptom amplification indicative of functional or psychogenic illness, while our group thinks that some CFS patients may have brain dysfunction.
      To further pursue our encephalopathy hypothesis, we did spinal taps on 31 women and 13 men fulfilling the 1994 case definition for CFS and on 8 women and 5 men serving as healthy controls.
      Our outcome measures were white blood cell count, protein concentration in spinal fluid and cytokines detectable in spinal fluid.
      We found that significantly more CFS patients had elevations in either protein levels or number of cells than healthy controls (30 versus 0%) and 13 CFS patients had protein levels and cell numbers that were higher than laboratory norms; patients with abnormal fluid had a lower rate of having comorbid depression than those with normal fluid.
      In addition, of the 11 cytokines detectable in spinal fluid, (i) levels of granulocyte-macrophage colony-stimulating factor were lower in patients than controls, (ii) levels of interleukin-8 (IL-8) were higher in patients with sudden, influenza-like onset than in patients with gradual onset or in controls and (iii) IL-10 levels were higher in the patients with abnormal spinal fluids than in those with normal fluid or controls.
      The results support two hypotheses : that some CFS patients have a neurological abnormality that may contribute to the clinical picture of the illness and that immune dysregulation within the central nervous system may be involved in this process.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15642984?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDoc
      Sum

    • Objective evidence of cognitive complaints in Chronic Fatigue Syndrome - A BOLD fMRI study of verbal working memory
      Lange G, Steffener J, Cook DB, Bly BM, Christodoulou C, Liu WC, Deluca J, Natelson BH, Department of Radiology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, 07103, USA : lange@njneuromed.org - Neuroimage. 2005 Jun;26(2):513-24. Epub 2005 Apr 7 - PMID: 15907308
      Individuals with Chronic Fatigue Syndrome (CFS) often have difficulties with complex auditory information processing.
      In a series of two Blood Oxygen Level Dependent (BOLD) functional Magnetic Resonance Imaging (fMRI) studies, we compared BOLD signal changes between Controls and individuals with CFS who had documented difficulties in complex auditory information processing (Study 1) and those who did not (Study 2) in response to performance on a simple auditory monitoring and a complex auditory information processing task (mPASAT).
      We hypothesized that under conditions of cognitive challenge : (1) individuals with CFS who have auditory information processing difficulties will utilize frontal and parietal brain regions to a greater extent than Controls and (2) these differences will be maintained even when objective difficulties in this domain are controlled for.
      Using blocked design fMRI paradigms in both studies, we first presented the auditory monitoring task followed by the mPASAT.
      Within and between regions of interest (ROI), group analyses were performed for both studies with statistical parametric mapping (SPM99).
      Findings showed that individuals with CFS are able to process challenging auditory information as accurately as Controls but utilize more extensive regions of the network associated with the verbal WM system.
      Individuals with CFS appear to have to exert greater effort to process auditory information as effectively as demographically similar healthy adults.
      Our findings provide objective evidence for the subjective experience of cognitive difficulties in individuals with CFS.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    • Detection of immunologically significant factors for chronic fatigue syndrome using neural-network classifiers
      Hanson SJ, Gause W, Natelson B, Department of Psychology, Rutgers University, Newark, New Jersey 07102, USA : jose@kreizler.rutgers.edu - Clin Diagn Lab Immunol. 2001 May;8(3):658-62 - PMID: 11329477
      Neural-network classifiers were used to detect immunological differences in groups of chronic fatigue syndrome (CFS) patients that heretofore had not shown significant differences from controls.
      In the past linear methods were unable to detect differences between CFS groups and non-CFS control groups in the nonveteran population.
      An examination of the cluster structure for 29 immunological factors revealed a complex, nonlinear decision surface.
      Multilayer neural networks showed an over 16% improvement in an n-fold resampling generalization test on unseen data.
      A sensitivity analysis of the network found differences between groups that are consistent with the hypothesis that CFS symptoms are a consequence of immune system dysregulation.
      Corresponding decreases in the CD19(+) B-cell compartment and the CD34(+) hematopoietic progenitor subpopulation were also detected by the neural network, consistent with the T-cell expansion.
      Of significant interest was the fact that, of all the cytokines evaluated, the only one to be in the final model was interleukin-4 (IL-4).
      Seeing an increase in IL-4 suggests a shift to a type 2 cytokine pattern.
      Such a shift has been hypothesized, but until now convincing evidence to support that hypothesis has been lacking.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    • Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome
      Peckerman A, LaManca JJ, Dahl KA, Chemitiganti R, Qureishi B, Natelson BH, Department of Neurosciences, CFS Cooperative Research Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA : apeckerm@njneuromed.org - Am J Med Sci. 2003 Aug;326(2):55-60 - PMID: 12920435
      Background
      - Findings indicative of a problem with circulation have been reported in patients with chronic fatigue syndrome (CFS).
      We examined this possibility by measuring the patient's cardiac output and assessing its relation to presenting symptoms.
      Methods - Impedance cardiography and symptom data were collected from 38 patients with CFS grouped into cases with severe (n = 18) and less severe (n = 20) illness and compared with those from 27 matched, sedentary control subjects.
      Results - The patients with severe CFS had significantly lower stroke volume and cardiac output than the controls and less ill patients.
      Postexertional fatigue and flu-like symptoms of infection differentiated the patients with severe CFS from those with less severe CFS (88.5% concordance) and were predictive (R2 = 0.46, P < 0.0002) of lower cardiac output.
      In contrast, neuropsychiatric symptoms showed no specific association with cardiac output.
      Conclusions - These results provide a preliminary indication of reduced circulation in patients with severe CFS.
      Further research is needed to confirm this finding and to define its clinical implications and pathogenetic mechanisms.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    • Chronic fatigue syndrome - The need for subtypes
      Jason LA, Corradi K, Torres-Harding S, Taylor RR, King C, DePaul University, Chicago, Illinois 60614, USA : ljason@depaul.edu - Neuropsychol Rev. 2005 Mar;15(1):29-58 - PMID: 15929497
      Chronic fatigue syndrome (CFS) is an important condition confronting patients, clinicians and researchers.
      This article provides information concerning the need for appropriate diagnosis of CFS subtypes.
      We first review findings suggesting that CFS is best conceptualized as a separate diagnostic entity rather than as part of a unitary model of functional somatic distress.
      Next, research involving the case definitions of CFS is reviewed.
      Findings suggest that whether a broad or more conservative case definition is employed and whether clinic or community samples are recruited, these decisions will have a major influence in the types of patients selected.
      Review of further findings suggests that subtyping individuals with CFS on sociodemographic, functional disability, viral, immune, neuroendocrine, neurology, autonomic and genetic biomarkers can provide clarification for researchers and clinicians who encounter CFS' characteristically confusing heterogeneous symptom profiles.
      Treatment studies that incorporate subtypes might be particularly helpful in better understanding the pathophysiology of CFS.
      This review suggests that there is a need for greater diagnostic clarity and this might be accomplished by subgroups that integrate multiple variables including those in cognitive, emotional and biological domains.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15929497?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVD
      ocSum



    Myth 2. - People with CFS who think they are suffering from a physical illness have a worse prognosis, which just goes to show that it is their perception of a physical cause for their illness that is keeping them from functioning normally

    It is more likely that people who think they are suffering from a physical illness have a worse prognosis because they are correct in recognizing that they have a physical illness, one that doctors do not yet have effective treatments for.

    Handbook of Chronic Fatigue Syndrome
    Leonard A. Jason, Patricia A. Fennell & Renee R - Wiley (June 26, 2003) – ISBN-10 : 047141512X / ISBN-13 : 978-0471415121
    'The Handbook of Chronic Fatigue Syndrome' provides authoritative coverage of Chronic Fatigue Syndrome (CFS).
    A leading group of international contributors present up-to-date information and guidance to improve the understanding, proper identification and treatment of this debilitating disease.
    The Handbook’s comprehensive, multidisciplinary format draws on the medical, as well as mental health — related, aspects of CFS, including :
    - History, diagnosis and classification
    - Phenomenology
    - Symptomatology
    - Assessment
    - Treatment and intervention
    - Pediatric and community issues.
    Topics covered include complexity of diagnosis, social effects of chronic disorders and a variety of treatment techniques, including phase-based therapy, cognitive-behavioral therapies, exercise therapy and nutritional approaches.
    An insightful and unique resource, the 'The Handbook of Chronic Fatigue Syndrome' is an enlightening book for all mental health professionals, including psychologists, social workers and counselors, as well as medical personnel, such as nurses, physicians and physical-occupational therapists.
    Cfr. :
    -
    http://www.amazon.com/Handbook-Chronic-Fatigue-Syndrome-Leonard/dp/047141512X
    -
    http://albanyhealthmanagement.com/books/handbook.html



    Myth 3. - Whenever one research group finds a biological abnormality in patients with CFS, another research group can't find it

    With research on virtually all illnesses, there are always some reports in the research literature that conflict.
    The question with CFS or any illness is : counting all of the published reports and the numbers of patients in all of these reports, do the great majority of reports involving the great majority of patients find objective biological abnormalities ?
    The answer for CFS, with regard to studies of the nervous system and immune system, is yes.

    • The Biology of Chronic Fatigue Syndrome
      Anthony L. Komaroff, M.D. - Harvard Health Publications, 10 Shattuck St. Suite 602, Boston, Mass 02115 USA : komaroff@hms.harvard.edu – Fax : 617 432-4719
      The Epidemiologic Context
      The presenting complaint of chronic fatigue is a very common cause of visits to a doctor.
      Very often, an underlying depression (often with accompanying anxiety) is the cause of chronic fatigue.
      In our experience, overwork is another very common cause.
      Well-defined organic conditions such as anemia, hypothyroidism and occult malignancy are the underlying cause chronic fatigue in a small fraction (2-5%) of cases.
      Chronic fatigue syndrome (CFS) is found in another small fraction of cases (2%).
      Symptoms
      CFS is an illness with a formal case definition that has been developed with the leadership of the Centers for Disease Control and Prevention.
      The illness is characterized by at least six months of exceptional fatigue, with several associated chronic symptoms : impaired memory or concentration, sore throat, tender cervical or axillary lymph nodes, muscle pain, multi-joint pain, new headaches, unrefreshing sleep, post-exertional malaise.
      Patients may be of any age, either sex and from all walks of life: the typical patient is a 35-year old white woman.
      Often, the onset is sudden, often following an acute "viral" syndrome.
      Some patients appear to be completely disabled by the symptoms.
      The impairment in functional status of patients with CFS, as measured by the SF-36 instrument, is comparable to that of patients with congestive heart failure.
      Past medical history is notable primarily for a high frequency of atopic or allergic illness (in approximately 50%-80%).
      Physical examination is notable for posterior cervical adenopathy in about 35%; and abnormal tests of balance (Romberg and tandem gait) in about 25%.
      Laboratory Tests
      No single laboratory test has been identified that has both high sensitivity and specificity for CFS; hence, there is no diagnostic test for CFS.
      However, a growing literature reports a number of objective laboratory findings that clearly distinguish patients with CFS from healthy control subjects (and, in some cases, from comparison group patients with various fatiguing psychiatric and organic diseases).
      In our experience, several findings are seen more often in patients with CFS : circulating immune complexes (low levels), elevated total complement (CH50), elevated IgG, atypical lymphocytosis and ANA (low levels).
      Neuroendocrine Findings
      Many studies have found that patients with CFS, in comparison with healthy control subjects, have a variety of abnormalities of the hypothalamic-pituitary axes.
      For example, there is reduced hypothalamic production of corticotropin releasing hormone, leading to diminished pituitary release of ACTH, leading to basal hypocortisolism.
      This axis abnormality is the opposite of what is seen in patients hospitalized for major, melancholic depression.
      A recent study, using CT, found that the adrenal glands of patients with CFS were half the size of adrenals from healthy control subjects.
      Neuroimaging
      Several different groups have reported that magnetic resonance imaging (MRI) reveals punctate areas of high signal in the white matter, particularly in the subcortical areas, more frequently than in age and gender-matched healthy control subjects.
      Nevertheless, these findings are neither very sensitive nor specific.
      MRI is not recommended for the diagnosis of CFS, although it can be useful in pursuing the diagnosis of multiple sclerosis.
      MS is sometimes in the differential diagnosis, since patients with MS often present with prominent fatigue, paresthesias, visual blurring and other symptoms suggestive of CFS and since some patients (about 10%, in our experience) with CFS have had a transient focal neurologic deficit.
      Single-photon emission tomography (SPECT) also reveals defects of perfusion and/or metabolism much more often in patients with CFS than in healthy control subjects.
      Depression also produces SPECT scan abnormalities; however, most studies indicate that SPECT abnormalities occur more often in CFS than in depression.
      SPECT is not recommended for the diagnosis of CFS.
      Autonomic Nervous System Testing. Studies from Johns Hopkins, Harvard and other institutions find evidence of both sympathetic and parasympathetic neuropathy in patients with CFS.
      Clinically, many patients meet criteria for neurally-mediated hypotension and postural tachycardia syndromes.
      Studies of Infectious Agents
      No infectious agent has been convincingly shown to be a cause of CFS, and most investigators think it is unlikely that a single novel agent is the cause.
      Nevertheless, there is evidence from several controlled studies of the reactivation of several chronic viral infections in CFS.
      In our opinion, the evidence is strongest for human herpesvirus-6, a neurotropic and immunotropic virus.
      CFS has been documented following a variety of acute infections with viruses (such as following acute infectious mononucleosis), bacteria (such as following properly-treated Lyme disease) and other microbial infections (such as following Q fever).
      Immunological Studies
      A variety of other immunologic abnormalities have been reported, especially impaired function of natural killer cells and increased numbers of activated CD8+ T cells.
      Neither of these two abnormalities, however, is adequately sensitive or specific to constitute a diagnostic test.
      They are consistent with the hypothesis that the immune system is chronically activated in patients with CFS.
      Recently, two groups have reported what appears to be a more specific immune system abnormality in CFS : increased activity of the 2-5A pathway enzymatic pathway in lymphocytes.
      Patients with CFS were very different from patients with major depression, fibromyalgia or healthy control subjects.
      Further studies are needed to determine if this test is adequately sensitive and specific to constitute a diagnostic test.
      At this time, it is still experimental.
      Psychiatric Issues
      Probably only a small fraction of patients who seek medical care for fatigue have CFS; most fatigued patients probably suffer from depression or overwork.
      Of the few patients with chronic fatigue who meet criteria for CFS, most become depressed and anxious after the onset of the illness and this depression and anxiety need to be recognized and treated, when present.
      Most patients with CFS have no prior history of significant psychiatric disease prior to the onset of CFS, according to several careful studies.
      However, at least 50% of patients develop depression, anxiety or other psychoneurotic disorders in the years after the onset of CFS.
      One randomized, placebo-controlled, double-blind trial of fluoxetine therapy in patients with CFS found no evidence of benefit : neither the fatigue nor the coexisting depression in some patients got better with fluoxetine.
      Treatment
      Treatment with low-dose tricyclics (e.g. amitriptyline, 10-20mg q.h.s.) has been proven efficacious in a randomized trial of a clinically similar condition (fibromyalgia) and is widely used in CFS.
      This treatment improves an objectively documented sleep disorder (alpha intrusion into delta wave sleep) seen in these conditions; results are apparent within days (not weeks) of initiating therapy.
      Such low doses of tricyclics do not appear to improve any coexisting depression.
      Recently, some improvement has been reported with the use of cognitive behavioral therapy, in skilled hands and with slowly graded aerobic exercise programs.
      What is CFS ?
      In our view, the evidence above indicates that CFS has an organic basis : in many (but not all) patients, there are abnormalities of the limbic system of the brain and abnormal regulation of the immune system (possibly as a result of limbic system abnormalities).
      A single cause seems unlikely; multiple different triggering agents (infectious agents, toxins, stress) could be involved in different cases.
      Cfr. :
      http://www.ahmf.org/01komaroff.html

    • Chronic fatigue syndrome - New insights and old ignorance
      Evengård B, Schacterle RS, Komaroff AL, Division of Infectious Diseases, Department of Immunology, Karolinska Institute at Huddinge University Hospital, Huddinge, Sweden : birgitta.evengardinfect.hs.sll@se - J Intern Med. 1999 Nov;246(5):455-69 - PMID: 10583715
      Chronic fatigue syndrome (CFS) is a condition characterized by impairment of neurocognitive functions and quality of sleep and of somatic symptoms such as recurrent sore throat, muscle aches, arthralgias, headache and postexertional malaise.
      A majority of patients describe an infectious onset but the link between infections and CFS remains uncertain.
      Findings show an activation of the immune system, abberations in several hypothalamic-pituitary axes and involvement of other parts of the central nervous system.
      The origin is bound to be complex and it may well be that the solution will come together with a more generally altered view about mind-body dualism and the concept of illness and disease.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/10583715



    Myth 4. - CFS only affects white and higher income individuals, and is a relatively rare disorder

    Recent evidence from community prevalence studies indicates that CFS is not a YUPPIE disease and in fact, it occurs more often among Latino and African-American minority groups and those with lower incomes.
    CFS affects from 800,000 to one million individuals in the US and thus represents one of the more common chronic health conditions.

    • Prevalence and incidence of chronic fatigue syndrome in Wichita, Kansas
      Reyes M, Nisenbaum R, Hoaglin DC, Unger ER, Emmons C, Randall B, Stewart JA, Abbey S, Jones JF, Gantz N, Minden S, Reeves WC, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Public Health Service, US Department of Health and Human Services, Atlanta, GA 30333, USA - Arch Intern Med. 2003 Jul 14;163(13):1530-6 - PMID: 12860574
      Background - Chronic fatigue syndrome (CFS) is a debilitating illness with no known cause or effective therapy.
      Population-based epidemiologic data on CFS prevalence and incidence are critical to put CFS in a realistic context for public health officials and others responsible for allocating resources and for practicing physicians when examining and caring for patients.
      Methods - We conducted a random digit-dialing survey and clinical examination to estimate the prevalence of CFS in the general population of Wichita, Kan and a 1-year follow-up telephone interview and clinical examination to estimate the incidence of CFS.
      The survey included 33 997 households representing 90 316 residents.
      This report focuses on 7162 respondents aged 18 to 69 years.
      Fatigued (n = 3528) and randomly selected nonfatigued (n = 3634) respondents completed telephone questionnaires concerning fatigue, other symptoms and medical history.
      The clinical examination included the Diagnostic Interview Schedule for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, laboratory testing and a physical examination.
      Resulsts - The overall weighted point prevalence of CFS, adjusted for nonresponse, was 235 per 100,000 persons (95% confidence interval, 142-327 per 100,000 persons).
      The prevalence of CFS was higher among women, 373 per 100,000 persons (95% confidence interval, 210-536 per 100,000 persons), than among men, 83 per 100,000 persons (95% confidence interval, 15-150 per 100,000 persons).
      Among subjects nonfatigued and fatigued for less than 6 months, the 1-year incidence of CFS was 180 per 100,000 persons (95% confidence interval, 0-466 per 100,000 persons).
      Conclusions - Chronic fatigue syndrome constitutes a major public health problem.
      Longitudinal follow-up of this cohort will be used to further evaluate the natural history of this illness.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/12860574

    • A community-based study of chronic fatigue syndrome
      Jason LA, Richman JA, Rademaker AW, Jordan KM, Plioplys AV, Taylor RR, McCready W, Huang CF, Plioplys S, Department of Psychology, DePaul University, Chicago, IL 60614, USA : ljason@wppost.depaul.edu - Arch Intern Med. 1999 Oct 11;159(18):2129-37 - PMID: 10527290
      Background - Most previous estimates of the prevalence of chronic fatigue syndrome (CFS) have derived largely from treated populations and have been biased by differential access to health care treatment linked with sex, ethnic identification and socioeconomic status.
      Objective - To assess the point prevalence of CFS in an ethnically diverse random community sample.
      Design and participants - A sample of 28,673 adults in Chicago, Ill, was screened by telephone and those with CFS-like symptoms were medically evaluated.
      Main outcome measures and analyses - Self-report questionnaires, psychiatric evaluations and complete medical examinations with laboratory testing were used to diagnose patients with CFS.
      Univariate and multivariate statistical techniques were used to delineate the overall rate of CFS in this population and its relative prevalence was subcategorized by sex, ethnic identification, age and socioeconomic status.
      Results - There was a 65.1% completion rate for the telephone interviews during the first phase of the study.
      Findings indicated that CFS occurs in about 0.42% (95% confidence interval, 0.29%-0.56%) of this random community-based sample.
      The highest levels of CFS were consistently found among women, minority groups and persons with lower levels of education and occupational status.
      Conclusions - Chronic fatigue syndrome is a common chronic health condition, especially for women, occurring across ethnic groups.
      Earlier findings suggesting that CFS is a syndrome primarily affecting white, middle-class patients were not supported by our findings.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/10527290



    Myth 5. - Cognitive behavior therapy interventions can cure CFS

    Cognitive behavior therapy is widely used to help people cope with chronic illnesses, both “physical” illnesses and psychological illnesses.
    While these types of psychological interventions can help patients with CFS cope better with their symptoms and deal with the consequences of having a chronic health problem, these types of intervention do not cure the illness.

    • Cognitive behavioral therapy as cure-all for CFS
      Elke Van Hoof, (2004) - Journal of Chronic Fatigue Syndrome, 11, 43-47
      Cfr. :
      http://www.voetbalacademie.be/VAN%20HOOF%20ELKE%20curriculum_vitae.htm
      Critical discussion paper noting some of the flaws of the Prins et al study and the fact that improvements reported by those having CBT often did not last.
      Cognitieve gedragstherapie bij het chronische vermoeidheidssyndroom (ME/CVS) vanuit het perspectief van de patiënt
      Drs. M.P. Koolhaas, H. de Boorder, Prof. Dr. E. van Hoof - februari 2008 – ISBN : 978-90-812658-1-2 - Digitale exemplaren van dit rapport kunnen besteld worden via : onderzoekcgt@live.nl
      Background
      - In recent years, Chronic Fatigue Syndrome, also known as Myalgic Encephalomyelitis (ME/CFS), has been getting a lot of attention in scientific literature.
      However its aetiology remains unclear and it has yet to be clarified why some people are more prone to this condition than others.
      Furthermore, there is as yet no consensus about the treatment of ME/CFS.
      The different treatments can be subdivided into two groups, the pharmacological and the psychosocial therapies.
      Most of the scientific articles on treatment emphasize the psychosocial approach.
      The most intensively studied psychological therapeutic intervention for ME/CFS is cognitive behaviour therapy (CBT).
      In recent years several publications on this subject have been published.
      These studies report that this intervention can lead to significant improvements in 30% to 70% of patients, though rarely include details of adverse effects.
      This pilot study was undertaken to find out whether patients’ experiences with this therapy confirm the stated percentages.
      Furthermore, we examined whether this therapy does influence the employment rates and could possibly increase the number of patients receiving educational training, engaged in sports, maintaining social contacts and doing household tasks.
      Method - By means of a questionnaire posted at various newsgroups on the internet, the reported subjective experiences of 100 respondents who underwent this therapy were collected.
      These experiences were subsequently analysed.
      Results - Only 2% of respondents reported that they considered themselves to be completely cured upon finishing the therapy.
      Thirty per cent reported ‘an improvement’ as a result of the therapy and the same percentage reported no change.
      Thirty-eight percent said the therapy had affected them adversely, the majority of them even reporting substantial deterioration.
      Participating in CBT proved to have little impact on the number of hours people were capable of maintaining social contacts or doing household tasks.
      A striking outcome is that the number of those respondents who were in paid employment or who were studying while taking part in CBT was adversely affected.
      The negative outcome in paid employment was statistically significant. CBT did, however, lead to an increase in the number of patients taking up sports.
      A subgroup analysis showed that those patients who were involved in legal proceedings in order to obtain disability benefit while participating in CBT did not score worse than those who were not.
      Cases where a stated objective of the therapy was a complete cure, did not have a better outcome. Moreover, the length of the therapy did not affect the results.
      Conclusions - This pilot study, based on subjective experiences of ME/CFS sufferers, does not confirm the high success rates regularly claimed by research into the effectiveness of CBT for ME/CFS.
      Over all, CBT for ME/CFS does not improve patients’ well-being: more patients report deterioration of their condition rather than improvement.
      Our conclusion is that the claims in scientific publications about the effectiveness of this therapy based on trials in strictly controlled settings within universities, has been overstated and are therefore misleading.
      The findings of a subgroup analysis also contradict reported findings from research in strictly regulated settings.
      Cfr. :
      http://www.medivera.nl/cgtbijmecvsvanuitperspectiefpatient2008.pdf



    Myth 6. - Patients with CFS are either lazy or malingering

    There is no truth to this statement and many patients with this condition would like nothing better than to have their old lifestyle back.
    They are very motivated and often go to many physicians to find a way of getting better.

    • Understanding Chronic Fatigue Syndrome - An Empirical Guide to Assessment and Treatment
      Fred Friedberg & Leonard Jason - American Psychological Association (APA) - 1 edition, August 1998 – ISBN-10 : 1557985111 / ISBN-13 : 978-1557985118
      Covers the physical and psychological aspects of chronic fatigue syndrome.
      Presents many cognitivebehavioral methods of treatment and gives an overview of the history, definition, prevalence and models of the illness.
      For clinicians, psychologists and psychoneuroimmunologists.
      Cfr. :
      http://www.amazon.com/Understanding-Chronic-Fatigue-Syndrome-Assessment/dp/1557985111



    Myth 7. - All cases of CFS are caused by the Epstein-Barr Virus (EBV)

    These are common misconceptions among primary care providers.
    The onset of CFS is sometimes but not always linked with the recent presence of an infection.
    CFS has been reported as following acute mononucleosis (a viral infection like EBV), Lyme disease (a bacterial infection) and Q fever (an infection with a different type of infectious agent).

    • The Physical Basis of CFS
      Anthony L. Komaroff, M.D., Professor of Medicine, Harvard Medical School and Editor-in-Chief Harvard Health Publications, Boston, Mass - Harvard Medical School - M E International – Source : this article appeared in the CFS Research Review, Spring 2000, Vol. 1 Issue 2, a quarterly newletter of the CFIDS Association of America, PO Box 220398, Charlotte, NC 28210. (704) 365-2343 and is © 2000 by the CFIDS Association of America
      Often, when people hear that there is no known test or cause for chronic fatigue syndrome (CFS), they mistakenly understand that to mean that the illness is not real.
      This is incorrect.
      Over the past 15 years, scientists have identified numerous biological abnormalities that provide evidence for the reality and seriousness of CFS, even though the cause of CFS and diagnostic tests for it are still unknown. (1)
      These biological abnormalities have given researchers clues to the cause of the illness.
      In particular, they have provided evidence that the illness involves both the brain and the immune system.
      There are no diagnostic tests yet for CFS because none of the biological abnormalities clearly distinguishes patients with CFS from other individuals.
      In reality, there are no perfect biological tests (see sidebar at end) for any illness.
      When a test gets close enough to perfect, clinicians use it to help confirm or refute their clinical judgment.
      Testing in CFS has primarily been used to rule out other illnesses that also can cause chronic fatigue.
      What is the cause of CFS ?
      The leading model of CFS pathogenesis is rooted in scientifically identified abnormalities in the brain (central nervous system) and the immune system, which influence and alter the function of the other in a reciprocal cycle (see Fig. 1).
      Low levels of circulating cortisol, identified in several CFS research studies (2,3) can increase immune activation, which is also a key feature of CFS.
      This immune system activation could theoretically result in brain dysfunction : when the immune system is activated, it makes chemical messages.
      Brain cells as well as other immune system cells can receive these messages.
      This could lead to fatigue, cognitive dysfunction, enhanced sense of pain, hormonal dysregulation and other features of CFS. (4)
      Post-viral onset
      Many cases of CFS cases begin with symptoms suggesting an infection, like a common viral illness.
      Doctors do not usually perform tests to confirm common viral infections, since they typically quickly resolve.
      For that reason, there is no documentation of the infection that seems to start CFS in many patients.
      However, some of the most interesting research in recent years involves studies that did document an infection at the start of the illness.
      For example, CFS has been reported following acute mononucleosis (5,6) (a viral infection), Lyme disease (7-9) (a bacterial infection) and Q fever (10) (an infection with a different kind of infectious agent).
      These studies prove that CFS can indeed follow in the wake of a well-documented infection.
      This research indicates that no single infectious agent is likely to be the cause of CFS.
      Instead, CFS is likely to be caused by some abnormality in the body’s response to any of several different infectious agents.
      The studies of infectious agents in CFS are complicated.
      One reason is that the symptoms of CFS almost surely arise from the brain, yet it is very hard for scientists to study infectious agents in the human brain : that requires taking brain tissue (biopsies), a potentially dangerous test.
      Another reason is that some infectious agents permanently live in a dormant state inside our bodies.
      There is evidence that some of these infections, like infection with the virus HHV-6, (11-14) get reawakened in patients with CFS.
      The unanswered question is whether the reawakened virus is the cause of the bodily damage and resulting symptoms, or whether it is result of the illness.
      Immune system abnormalities
      Several immune system patterns are seen more often in patients with CFS.
      The identified abnormalities mimic the immune pattern of a body fighting a virus, even though no virus has been identified as the cause of CFS.
      Specific findings include :
      - increased numbers of CD8+ activated “cytotoxic” T cells (cells commonly increased when the body is fighting viral infections) (11,15-17)
      - low natural killer cell function (18-21)
      - eevated immune complexes. (22)
      The most intriguing recent immunological finding in CFS is the discovery of a novel, low molecular weight protein in an antiviral pathway called the RNase-L pathway. (24-27)
      This novel protein is found much more often in CFS patients than in healthy people, or people with two other conditions that can cause fatigue : depression or fibromyalgia. (27)
      Neurological findings
      There is considerable evidence that the brain and central nervous system are involved in CFS.
      Soft” evidence includes patient-reported symptoms such as: cognitive dysfunction; sensitivities to stimuli such as bright lights, noise and odors; numbness and tingling in the extremities; and disordered and fragmented sleep.
      Hard” evidence includes :
      - hyperintense signals on MRI scans (11,28,29)
      - reduction in cerebral blood flow on SPECT scans—an abnormality that changes over time and is not an indication of any permanent brain damage (30,31)
      - autonomic dysfunction, primarily orthostatic intolerance and neurally mediated hypotension seen on tilt table tests; (32-37) the control centers for maintenance of blood pressure lie in the brain’s limbic system.
      - epidemiology - recent epidemiological data has helped to establish the relevance and importance of CFS as a serious public health issue; data from private investigators and from the Centers for Disease Control and Prevention (CDC) indicate that more than 200 of every 100,000 Americans have CFS (38-40)
      - depending on demographic factors - such as age, sex and ethnicity - the prevalence can range from 200 to 800 cases per l00,000; (38) this makes CFS more common than well-known illnesses such as multiple sclerosis (41) and systemic lupus erythematosus (42), which, like CFS, predominantly affect females.
      CFS is real
      Taken together, these and other findings provide important evidence that CFS is not “all in the head” or an imagined illness.
      While there is not yet a test, scientists are moving closer to developing tools to assist clinicians in the diagnosis of CFS.
      In the interim, scientists have provided clues to the biology of CFS and have given clinicians, scientists and patients critical data that shows that CFS is a real and serious illness.
      References
      1 - The biology of chronic fatigue syndrome
      Komaroff AL - Am J Med. 2000;108:169-71
      2 - Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome
      Demitrack MA et al. - J din Endo Metab. 199173(6): 1224-1234
      3 - Urinary free cortisol excretion in depression, in chronic fatigue syndrome and in health
      Scott LV, Dinan T - JAffect Disord. 1998; 47:49-54
      4 - Stroke therapy
      Zivin JA, Choi DW. S - Scient,jic American. July 1991 ;265:56-63
      5 - Evidence for active Epstein-Barr virus infection in patients with persistent, unexplained illnesses - Elevated anti-early antigen antibodies
      Jones JF et al. - Ann Intern Med. 1985; l02( 1): 1-7
      6 - Persisting illness and fatigue in adults with evidence of Epstein-Barr virus infection
      Straus SE et al. - Ann Intern Med. 1985;2(l):7-l6
      7 - Summary of the first 100 patients seen at a Lyme disease referral center
      Sigal LH - Am J Med. 1990;88:577-81
      8 - The overdiagnosis of Lyme disease
      Steere AC et al - JAMA. 1993; 269:1812-16
      9 - Borrelia burgdorferi reactivity in patients with severe persistent fatigue who are from a region where Lyme disease is endemic
      Coyle PK et al. - Cl/n Infect Din. l994;18:S24-7
      10 - Protracted debility and fatigue after acute Q fever
      Marmion BP et al. - Lancet. T996;347:977-8
      11 - A chronic illness characterized by fatigue, neurologic and immunologic disorders and active human herpesvims type.6 infection
      Buchwald D et al. - Ann Intern Med. 1992;ll6:106-13
      12 - Prevalence of human herpesvirus 6 variants A and B in patients with chronic fatigue syndrome
      Yalcin S et al. - Microbiol Insmunol. 1 994;38:587-90
      13 - Active HHV-6 infection in chronic fatigue syndrome patients from Italy - New data
      Zorzenon Metal - J CFS. 1996;2(l):3-l2
      14 - Prevalence of 1gM antibodies to human herpesvirus 6 early antigen (p41/38) in patients with chronic fatigue syndrome
      Patnaik M et al. - J of Infect Dis. 1995;l72:1364-1367
      15 - Immunological abnormalities in the chronic fatigue syndrome
      Lloyd et al. - Med J Austral. 1989; 15 1: 122-4
      16 - Chronic fatigue syndrome: clinical condition associated with immune activation
      Landay AL et al. - Lancet.199l;338: 707-12
      17 - Immunologic abnormalities in chronic fatigue syndrome
      Klimas NG et al. - J C/in Microbiol. 1990;28:1403-l0
      18 - Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome
      Caligiuri M et al. - J Immunol. 1987;139:3306-l3
      19 - A comprehensive immunological analysis in chronic fatigue syndrome
      Gupta S, Vayuvegula B - Scand J Immunol. 1991; 33:319-27
      20 - Natural killer cells and natural killer cell activity in chronic fatigue syndrome
      Whiteside TL, Friberg D - AmJMed. 1998;105(3A) :27S-34S
      21 - Natural killer cell activity in the chronic fatigue immune dysfunction syndrome
      Eby Net al. - In : 'Natural Killer Cells and Host Defense' - Ades EW, Lopes C, eds. 1988; 14 1-45
      22 - Clinical laboratory test findings in patients with chronic fatigue syndrome
      Bates DW et al. - Arch Intern Med. 1995;155;97-103
      23 - Biochemical evidence for a novel low molecular weight 2-5A-dependent RNase L in chronic fatigue syndrome
      Suhadolnik RJ et al. - J Interfernn Cytokine Res. 1997;17(7): 377-85
      24 - Changes in the 2-5A synthetase/RNase L antiviral pathway in a controlled clinical trial with poly(I)poly(CI2U) in chronic fatigue syndrome
      Suhadolnik RJ et al. - In Vivo. 1994; 8(4): 599-604
      25 - Upregulation of the 2-5A synthetase/RNase L antiviral pathway associated with chronic fatigue syndrome
      Suhadolnik RJ et al. - Clin Infect Di,s. t994;l8(l):S96-I04
      26 - A 37 kDa 2-5A binding protein as potential biomarker for chronic fatigue syndrome
      De Meirleir K et al. - AmJMed. 2000;108: 99-105
      27 - A controlled study of brain magnetic resonance imaging in patients with the chronic fatigue syndrome
      Natelson BH Ct al. - J Neurol Sci. L993;120(2):21 3-7
      28 - Brain MRI abnormalities exist in a subset of patients with chronic fatigue syndrome
      Lange G et al. - JNeurol Sci. 1999;I71(l):37
      29 - SPECT imaging of the brain - Comparison of findings in patients with chronic fatigue syndrome, AIDS dementia complex and major unipolar depression
      Schwartz RB et al. - Am J Roentgenol.l994; l62(4):943-51
      30 - Assessment of regional cerebral perfusion by 99Tcm-HMPAO SPECT in chronic fatigue syndrome
      Ichise Metal - NucI Med Commun. 1992;13(l0): 767-72
      31 - Is neurally mediated hypotension an unrecognized cause of chronic fatigue ?
      Rowe PC et al. - Lancet. 1995;345:623-4
      32 - The relationship between neurally mediated hypotension and the chronic fatigue syndrome
      Bou-Houlaigah I et al. - JAMA. 1995;274:96l-67
      33 - Orthostatic intolerance in the chronic fatigue syndrome
      Schondorf R et al. - J Auton Ner Syst. 1999; 75: 192-201
      24 - Does the chronic fatigue syndrome involve the autonomic nervous system ?
      Freeman R, Komaroff AL - Am J Med. 1997;104:957-64
      35 - Pathogenesis and management of delayed orthostatic hypotension in patients with chronic fatigue syndrome
      Dc Lorenzo F et al. - Clin Auton Res. 1997;7:185-90
      36 - The role of delayed orthostatic hypotension in the pathogenesis of chronic fatigue
      Streeten DHP, Anderson OH Jr. - Clin Autonom Res. L998;8: 11924
      37 - Wichita population-based study of a fatiguing illness
      Reyes M et al. - Presented at the American Association for Chronic Fatigue Syndrome Fourth International Research Conference. Cambridge, Mass., October 12, 1998. New Englandf Med in press
      38 - A community-based study of chronic fatigue syndrome
      Jason LA et al. - Arch Int Med. l999;159:2l29-37
      39 - Chronic Fatigue Syndrome Program Review - Objective I. - Surveillance
      Centers for Disease Control and Prevention, November 1999
      40 - Multiple Sclerosis - Hope Through Research
      National Institute of Neurological Diseases and Stroke (NINDS) - National Institutes of Health, I 999
      Cfr. :
      http://www.ninds.nih.gov/health_and_medical/pubs/multiple_sclerosis.htm
      41 - Lupus Erythemafosus
      National Institute of Allergy and Infectious Diseases (NIAID) - National Institutes of Health, 1999
      Cfr. :
      http://www.nih.gov/niams/healthinfo/Iupusguide/chp1.htm -.
      Cfr. :
      http://uk.geocities.com/me_not_cfs/The-Physical-Basis-of-CFS.html



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    CFS Myths

    Part II


    Myth 8. - Patients with CFS can be cured by exercise

    It is a myth that patients with CFS can be cured by exercise, but it is also a myth that no one with CFS can ever benefit from some physical activity.
    For some patients, a carefully monitored program incorporating paced and non-fatiguing activity can be used to strengthen and condition muscles.
    But it is worth noting that Black, O’Connor and McCully (2005) recently found that with an average 28% increase over baseline levels of daily physical activity over for a four week period, patients with CFS indicated they had worsening overall mood, muscle pain intensity and time spent each day with fatigue.

    • Increased daily physical activity and fatigue symptoms in chronic fatigue syndrome
      Black CD, O'connor PJ, McCully KK, Department of Exercise Science, The University of Georgia, Athens, GA, USA : kmccully@coe.uga.edu - Dyn Med. 2005 Mar 3;4(1):3 - PMID: 15745455
      Individuals with chronic fatigue syndrome (CFS) have been shown to have reduced activity levels associated with heightened feelings of fatigue.
      Previous research has demonstrated that exercise training has beneficial effects on fatigue-related symptoms in individuals with CFS.
      Purpose - The aim of this study was to sustain an increase in daily physical activity in CFS patients for 4 weeks and assess the effects on fatigue, muscle pain and overall mood.
      Methods - Six CFS and seven sedentary controls were studied.
      Daily activity was assessed by a CSA accelerometer.
      Following a two week baseline period, CFS subjects were asked to increase their daily physical activity by 30% over baseline by walking a prescribed amount each day for a period of four weeks.
      Fatigue, muscle pain and overall mood were reported daily using a 0 to 100 visual analog scale and weekly using the Profile of Mood States (Bipolar) questionnaire.
      Results - CFS patients had significantly lower daily activity counts than controls (162.5 +/- 51.7 x 103 counts/day vs. 267.2 +/- 79.5 x 103 counts/day) during a 2-week baseline period.
      At baseline, the CFS patients reported significantly (P < 0.01) higher fatigue and muscle pain intensity compared to controls but the groups did not differ in overall mood.
      CFS subjects increased their daily activity by 28 +/- 19.7% over a 4 week period.
      Overall mood and muscle pain worsened in the CFS patients with increased activity.
      Conclusion - CFS patients were able to increase their daily physical activity for a period of four weeks.
      In contrast to previous studies fatigue, muscle pain and overall mood did not improve with increased activity.
      Increased activity was not presented as a treatment which may account for the differential findings between this and previous studies.
      The results suggest that a daily "activity limit" may exist in this population.
      Future studies on the impact of physical activity on the symptoms of CFS patients are needed.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15745455

    • Exercise therapy for chronic fatigue syndrome
      Edmonds M, McGuire H, Price J - Cochrane Database Syst Rev. 2004;(3):CD003200 - PMID: 15266475
      Background
      - Chronic fatigue syndrome (CFS) is an illness characterised by persistent medically unexplained fatigue.
      CFS is a serious health-care problem with a prevalence of up to 3%.
      Treatment strategies for CFS include psychological, physical and pharmacological interventions.
      Objectives - To investigate the relative effectiveness of exercise therapy and control treatments for CFS.
      Search strategy - CCDANCTR-Studies and CENTRAL were searched using "Chronic Fatigue" and Exercise.
      The Journal of Chronic Fatigue Syndrome and CFS conferences were handsearched.
      Experts in the field were contacted.
      Clinicaltrials.gov and controlled-trials.com were searched.
      Selection criteria - Only Randomised Controlled Trials (RCT) including participants with a clinical diagnosis of CFS and of any age were included.
      Data collection and analysis - The full articles of studies identified were inspected by two reviewers (ME and HMG).
      Continuous measures of outcome were combined using standardised mean differences.
      An overall effect size was calculated for each outcome with 95% confidence intervals.
      One sensitivity analysis was undertaken to test the robustness of the results.
      Main results - Nine studies were identified for possible inclusion in this review and five of those studies were included.
      At 12 weeks, those receiving exercise therapy were less fatigued than the control participants (SMD -0.77, 95% CIs -1.26 to -0.28).
      Physical functioning was significantly improved with exercise therapy group (SMD -0.64, CIs -0.96 to -0.33) but there were more dropouts with exercise therapy (RR 1.73, CIs 0.92 to 3.24).
      Depression was non-significantly improved in the exercise therapy group compared to the control group at 12 weeks (WMD -0.58, 95% CIs -2.08 to 0.92).
      Participants receiving exercise therapy were less fatigued than those receiving the antidepressant fluoxetine at 12 weeks (WMD -1.24, 95% CIs -5.31 to 2.83).
      Participants receiving the combination of the two interventions, exercise + fluoxetine, were less fatigued than those receiving exercise therapy alone at 12 weeks, although again the difference did not reach significance (WMD 3.74, 95% CIs -2.16 to 9.64).
      When exercise therapy was combined with patient education, those receiving the combination were less fatigued than those receiving exercise therapy alone at 12 weeks (WMD 0.70, 95% CIs -1.48 to 2.88).
      Reviewer's conclusions - There is encouraging evidence that some patients may benefit from exercise therapy and no evidence that exercise therapy may worsen outcomes on average.
      However the treatment may be less acceptable to patients than other management approaches, such as rest or pacing.
      Patients with CFS who are similar to those in these trials should be offered exercise therapy and their progress monitored Further high quality randomised studies are needed.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/15266475



    Myth 9. - CFS is difficult to diagnose

    Actually it is pretty straightforward to diagnose when familiar with the case definition.
    It is, however, important to determine whether the Fukuda et al. (1994) or the Canadian case definition of ME/CFS is being used (Caruthers et al., 2003).

    • The chronic fatigue syndrome - A comprehensive approach to its definition and study
      International Chronic Fatigue Syndrome Study Group - Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333 - Ann Intern Med. 1994 Dec 15;121(12):953-9 - PMID: 7978722
      The complexities of the chronic fatigue syndrome and the methodologic problems associated with its study indicate the need for a comprehensive, systematic and integrated approach to the evaluation, classification and study of persons with this condition and other fatiguing illnesses.
      We propose a conceptual framework and a set of guidelines that provide such an approach.
      Our guidelines include recommendations for the clinical evaluation of fatigued persons, a revised case definition of the chronic fatigue syndrome and a strategy for subgrouping fatigued persons in formal investigations.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/pubmed/7978722

    • Myalgic encephalomyelitis/chronic fatigue syndrome - Clinical working case definition, diagnostic and treatments protocols
      Carruthers, B.M., Jain, A.K., DeMeirleir, K.L., Peterson, D.L., Klimas, N.G., Lerner, A.M., Bested, A.C., Flor-Henry, P., Joshi, P., Powles, A.C.P., Sherkey, J.A., & van de Sande, M.I. (2003).. Journal of Chronic Fatigue Syndrome, 11, 7-115
      Cfr. :
      http://www.cfids-cab.org/MESA/ccpccd.pdf


    Cfr. : http://www.iacfsme.org/Portals/0/pdf/myths.pdf


    10-03-2009 om 00:00 geschreven door Jules

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    09-03-2009
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Prevalence of Fibromyalgia - A Survey in Five European Countries
    Klik op de afbeelding om de link te volgen


    Prevalence of Fibromyalgia
    - A Survey in Five European Countries -

    Branco JC, Bannwarth B, Failde I, Abello Carbonell J, Blotman F, Spaeth M, Saraiva F, Nacci F, Thomas E, Caubère JP, Le Lay K, Taieb C, Matucci-Cerinic M, Department of Rheumatology, Hospital Egas Moniz, Lisboa, Portugal - Semin Arthritis Rheum. 2009 Feb 26. (Epub ahead of print) - PMID: 19250656


    Objective
    - A survey was performed in 5 European countries (France, Germany, Italy, Portugal and Spain) to estimate the prevalence of fibromyalgia (FM) in the general population.

    Methods - In each country, the London Fibromyalgia Epidemiological Study Screening Questionnaire (LFESSQ) was administered by telephone to a representative sample of the community over 15 years of age.
    A positive screen was defined as the following :
    (1) meeting the 4-pain criteria alone (LFESSQ-4) or
    (2) meeting both the 4-pain and the 2-fatigue criteria (LFESSQ-6).
    The questionnaire was also submitted to all outpatients referred to the 8 participating rheumatology clinics for 1 month.
    These patients were examined by a rheumatologist to confirm or exclude the FM diagnosis according to the 1990 American College of Rheumatology classification criteria.
    The prevalence of FM in the general population was estimated by applying the positive-predictive values to eligible community subjects (ie, positive screens).

    Results - Among rheumatology outpatients, 46% screened positive for chronic widespread pain (LFESSQ-4), 32% for pain and fatigue (LFESSQ-6) and 14% were confirmed FM cases.
    In the whole general population, 13 and 6.7% screened positive for LFESSQ-4 and LFESSQ-6, respectively. 3
    The estimated overall prevalence of FM was 4.7% (95% CI: 4.0 to 5.3) and 2.9% (95% CI : 2.4 to 3.4), respectively, in the general population.
    The prevalence of FM was age- and sex-related and varied among countries.

    Conclusion - FM appears to be a common condition in these 5 European countries, even if data derived from the most specific criteria set (LFESSQ-6) are considered.

    Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/19250656


    09-03-2009 om 11:24 geschreven door Jules

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