[Return to digest index] --------------------------------------------- This is a special digest of Co-Cure Research & Medical posts only Problems? Write to firstname.lastname@example.org --------------------------------------------- ---------------------------------------------------------------------- Date: Tue, 10 Jul 2007 14:26:18 -0400 From: Fred Springfield <fredspringfield1 VERIZON.NET> Subject: RES: Symptoms of autonomic dysfunction in chronic fatigue syndrome Symptoms of autonomic dysfunction in chronic fatigue syndrome. Journal: QJM. 2007 Jul 7; [Epub ahead of print] Authors: Newton JL, Okonkwo O, Sutcliffe K, Seth A, Shin J, Jones DE. Affiliation: From the Fatigue Interest group and Liver Research Group, Institute for Cellular Medicine, University of Newcastle, Newcastle, UK. NLM Citation: PMID: 17617647 BACKGROUND: Chronic fatigue syndrome (CFS) is common and its cause is unknown. AIM: To study the prevalence of autonomic dysfunction in CFS, and to develop diagnostic criteria. DESIGN: Cross-sectional study with independent derivation and validation phases. METHODS: Symptoms of autonomic dysfunction were assessed using the Composite Autonomic Symptom Scale (COMPASS). Fatigue was assessed using the Fatigue Impact Scale (FIS). Subjects were studied in two groups: phase 1 (derivation phase), 40 CFS patients and 40 age- and sex-matched controls; phase 2 (validation phase), 30 CFS patients, 37 normal controls and 60 patients with primary biliary cirrhosis. RESULTS: Symptoms of autonomic dysfunction were strongly and reproducibly associated with the presence of CFS or primary biliary cirrhosis (PBC), and correlated with severity of fatigue. Total COMPASS score >32.5 was identified in phase 1 as a diagnostic criterion for autonomic dysfunction in CFS patients, and was shown in phase 2 to have a positive predictive value of 0.96 (95%CI 0.86-0.99) and a negative predictive value of 0.84 (0.70-0.93) for the diagnosis of CFS. DISCUSSION: Autonomic dysfunction is strongly associated with fatigue in some, but not all, CFS and PBC patients. We postulate the existence of a 'cross-cutting' aetiological process of dysautonomia-associated fatigue (DAF). COMPASS >32.5 is a valid diagnostic criterion for autonomic dysfunction in CFS and PBC, and can be used to identify patients for targeted intervention studies. [Return to top] ------------------------------ Date: Wed, 11 Jul 2007 19:14:54 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: act,med: Letters re. NHS Clinics - July 2007 -(RiME) ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 11 July 2007 <<<< Editorship : Jan van Roijen Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ PERMISSION TO REPOST Campaigning for Research into ME (RiME) ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Letters re. NHS Clinics - July 2007 Ref: 602 Leader of Kent Maidstone Group Dear Dr Turner, I am writing to you in your capacity as Chairman of the APPG on ME. I attended the CBT clinic in Maidstone and do not believe that it offers anything to those with neurological conditions like ME. Those members of our Group I have spoken to feel that that money would be far better spent on biomedical research instead of psychiatric treatment offered by the Kent clinics. At the APPG meeting of 22 February 2007, I sent a message stating that our Group welcomed the fact that the APPG recognized ME as a neurological illness, as defined by ICD 10 G93.3, and asked if you were aware that the Kent clinic should by definition exclude patients who meet this criteria. People with ME in Kent are not concerned about being excluded, but are worried that the service offered by the clinics is not about their condition (ie neurological ICD-ME). I enclose letters from people who are boycotting them for this reason, as they do not want funding of them to continue. Is it possible to let parties other than MEA and AfME, despite their much smaller membership, have their say at future APPG meetings, and include those who can not attend because of their condition, to have their say by proxy? I ask that at the APPG meeting on 12 July 2007, that the Group discuss biomedical research and not the NHS clinics which offer the wrong kind of treatment entirely. May I also request that you read these points out at the meeting? I look forward to hearing from you. Ref: 550 Lancs For the past twelve years there has been a CFS clinic at North Manchester General Hospital run by four specialists who believe ME is a biological illness. The clinic has taken referrals from all over the North West of England. When the Manchester CNCC on CFS/ME was set up two years ago a psychiatrist, unknown to me, who also works at North Manchester General got the job of Clinical Champion. The four local specialists who believe ME is a biological illness were never even told that the job of Clinical Champion was available until AFTER the post was filled. The Manchester Psychiatrist Clinical Champion is now also chair of the whole English CNCC on CFS/ME collaborative. At the launch meeting for the Manchester CNCC he quoted only the psychosocial theory of ME. I have the lecture slides to prove this. At the lecture he expressed the psychosocial dogma that doctors who believe ME is a biological illness are an obstacle to the recovery of ME sufferers. When I asked him at a committee meeting to confirm if he truly believed in this dogma he refused to answer. I have just been told that after twelve years the CFS clinic run by the specialists who believe ME is a biological illness is to be closed and the psychiatrist is to get all the money that used to go to the running of the clinic. People in Greater Manchester will no longer have access to an NHS specialist who believes ME is a biological illness. This is all thanks to the new CNCC on CFS/ME set up. In future we will only have access to a service controlled by a psychiatrist who believes ME is a psychosocial illness. I am horrified that the Chair of the CNCC on CFS/ME Collaborative for the whole of England is a psychiatrist who believes ME is a psychosocial illness and is opppsed to doctors who believe ME is a biological illness. The Chair of the Collaborative is in charge of training and education for all the CNCCs on CFS/ME... Ref: 604 Yorks (Castleford) Dear Dr Turner, ... father of a young ME Sufferer aged 25 who has suffered from ME for the past 15 years. During this time she has had to put up with disbelief from the medical and educational establishments. Various management theories and treatments have been suggested and tried all to no avail; some have had short term benefits but nothing lasting. Even counselling at the Leeds CFS Clinic, to help her come to terms with her fatigue has not been of such a great benefit, she still suffers from the physical aspects of ME, and the pain and depression that goes with the continues ignoring of the fact that what is really needed It is with the past in mind that I consider the £8.5 million spent on such management would have been far better spent on biomedical research. I would be grateful if you would mention this at the APPG Meeting on July 12 2007... Ref: 605 Yorks (Leeds) Dear Dr Turner, I am writing to you in your capacity as Chair of the APPG on ME, and the meeting July 12 which will discuss the issue of the NHS 'CFS/ME' Clinics. The Leeds CNCC has nothing to offer people with genuine ME. I haven't attended nor has anyone else I know with ME. I enclose information about the 2006 Florida Conference. How much longer can the UK Government ignore the overwhelming evidence which indicates physical damage in ME patients? ME needs proper biomedical research not more psychiatric treatment ie Graded Exercise/CBT programmes. Since I will be unable to attend July 12 because of the ME, I ask that you include these points by proxy... Ref: 607 Derbys ... I was the leader of MEND (North Derbys ME group) from 1992 through the 1990's. It had a membership of 250. Please note that the title of the Group was Myalgic Enacephalomyelitis (ME). The only way forward to help people with ME is proper research into the physical causes and disease process of the neurological illness ME, as defined by WHO G.93.3 and the Canadian Criteria. Re. the new centres which have been set up: The nearest is the Sheffield CNCC which offers CBT - P.35 of 'CFS/ME Service Investment Program Report 2004-6', authored by Prof. Pinching + Pat Noons, (enclosed) - I can't relate to it at all. Not only is this form of treatment inappropriate to ME patients, but I feel the results will be 'skewed' (imprecise admittance criteria) and used by the Government as an excuse not to research the physical causes of ME. Is it not ironic that this meeting is not about the former - ME Research - but psychiatric/psychological models of treatment which are not helpful to people with ME? Please read this out July 12, if you have the opportunity. Ref: 609 Leics Dear Dr Turner, The East Midlands CNCC is not about neurological ICD-ME and offers same old, same old... I think there is a problem in that the APPG gives too much weight to what the MEA and AfME say on matters such as the clinics. Many who don't subscribe to the above (the vast majority with ME) would like to be at the APPG meeting July 12 to (1) challenge the nature of the 'CFS/ME' clinics (2) ask that the £8.5m be diverted into biomedical research. Since I will be able to attend, would you please read out thses points on my behalf... Ref: 612 Bucks Dear Dr Turner, I am writing to you in your role as Chair of the All Party Parliamentary group on ME. From 1989-94, as secretary to the Beds/Herts Group, whose membership averaged 450-500, I met many whose career had been suspened if not ended and lives ruined by the physical consequences of ME. From (a) listening to the experiences of members of this group (b) professional experience (NHS physiotherapist) (c) personal experience of ME, I am convinced of the potentially damaging effects of exercise and/or psycho-therapeutically based management of ME. Re. the centres which are currently being set up, the nearest seems to be the clinic at Barts in London. I don't deem the types of treatment which are being practiced there ie Graded Exercise and CBT as an appropriate way forward for patients with the neurological illness ME. There is ample and irrefutable evidence of the physical basis of ME. Do you think it shameful that the British Govt lags behind countries such as Chile and Latvia in promoting and supporting research into the physical causes of ME, so these patients have a chance to recover and resume a useful position in society? This, in my opinion, is what the APPG should currently be discussing. Since I am unable to attend the next APPG meeting July 12, would you please make these points by proxy... Ref: 615 Cornwall ... The clinics in the West country are ****. I hope the ME issue, like the property crisis, will lend weight to the Cornish Independence Movement. We pay tax to the Treasury at Westminster, and what do we get in return? Clinics run by psychiatrists and psychologists, and the stupid PACE + FINE Trials. Just think, if we had a Cornish Parliament we could have a say in how those taxes are spent; hopefully, a biomedical ME Research program... Pleased you are going to Westminster and raising people's concerns re. the clinics. Aren't there any people in London/South East who can support you... Ref: 617 Surrey Dear Dr Turner, I sent the enclosed to a number of MPs last June: .... In May you asked the Secretary of State for Health a question about the new NHS 'CFS/ME' Centres... The nearest to me is Sutton. The job description... appeared on AfME's website, last year (see RiME Newsletter, Spring 2005). Do you really think that the above will help with the neurological illness ME, and that it is worth saving? Do you not think that ME might be being confused with something else? One wonder if politicians are paying sufficient to the crucial issue of nomenclature... If you want to help people with ME, I suggest your next PQ is about why the Govt is not researching the underlying physical causes of ME... A year on, there is little I can add to these points. I sincerely hope the funding for the 'CFS/ME' Clinics does run out. I would like to see the money diverted into biomedical ME Research. I won't be able to attend the meeting July 12, so please make this point in my absence... Ref: 618 London (Greenwich) Dear Dr Turner, I fail to see how CNCCs like the one at Barts will help people with neurological ICD-ME. Let's compare what is in its leaflet 'The Chronic Fatigue Service' to the NICE Draft Guidelines: Barts Leaflet: GET: GET is about gradually increasing your physical activity. Usually you see a physiotherapist who helps you work out a basic activity routine, then together you plan to gradually increase the amount of physical activity or exercise you do... NICE: GET: 220.127.116.11: Adults... should be offered a program that includes planned increases in duration of physical activity/exercise followed by increases in intensity leading to aerobic exercise.... Other clinics eg Kent also prescribe GET. A leaflet entitled West Kent Chronic fatigue Service refers patients to Trudie Chalder's book, 'Coping with Chronic Fatigue' (didn't you sign a document - The Gibson Report - which descbibed her work 'impressive'?) which says Ch.6, 'Exercise three times a week, half an hour of exercise. Make sure it is something you enjoy. A brisk walk in the country is enough... ' Also: Base-Line Activity: NICE: 18.104.22.168: Managing setbacks: During a setback, when there is an increase in CFS/ME symptoms or symptoms are exacerbated, exercise or physical activity should be maintained if possible to avoid the negative effects of de-conditioning and withdrawal form activity.... Are you aware that rigid base-lines are being implemented via the NHS Clinics eg a person who attended the Maidstone Clinic says, ' .... Our individual baseline was then set at whatever we'd managed that week, with instructions to maintain it at that level. This wasn't at all successful as a number of the group then pushed themselves for the following two weeks, to their detriment'. Dr Turner, didn't you condemn the NICE Guidelines, 'no use to man nor beast' (APPG Meeting Nov. '06) but support the 'CFS/ME' Clinics per se (House of Commons 6/3/06)? In which case are there not anomalies that need addressing? I would like to be there July 12 to put these points to you to you directly but, as I will be unable to, would you please raise them by proxy, and then address them. I ask for a reply, also, in writing please... Ref: 620 Kent (Isle of Grain) In January 2003 I had an appointment to attend the Maidstone Clinic (Maidstone is approx 25 miles from where I live). The Chronic Fatigue Clinic was situated away from the hospital next to the psychiatric unit. I was interviewed twice to assess whether I was suitable for CBT. At the time I was not aware of being assessed for CBT, but found out later. I did not want to go as, having had ME 11 years, I was pacing and adjusting my life style to compensate for the ME. However, if I did not go I could never cite or say what happened. In January 2004 I was given an appointment at Medway Maritime Clinic (14 miles from home); I could drive there and park in the disabled bays. I certainly was not ready for the trek through Medway hospital to the appointed room; by the time I reached the room I was in pain, exhausted and a bit out of it. Undeterred, I stayed; the room started to fill up with other ME people, filling up the uncomfortable chairs. There must have been about 15 of us and, at the time, I thought it very strange that a CBT session should be a group as CBT is personal and everyone is an individual and will have different problems; some will be to shy to share; others will dominate the group and the whole thing will become ineffectual; as people needs are not met they will not come again and fall through the net, which did happen. The session started the same as any other group, name introduction act. There were three leaders: a lady who ran the session, a physiotherapist and a nurse. I am not sure why they were there as they did not do much. We were all asked our goals and aspirations, and what we would like to gain from this experience. Some of the answers saddened me, as people would say I would like to get better from having CBT, others just wanted some relief. Personally, I wanted less pain and exhaustion. I asked about pain control and was told there was none. The monthly sessions entailed forms to be filled in at home on our pacing methods. If you know anything about ME trying to fill in forms when you have cognitive fog just does not happen. When I am ill I cannot write a letter let alone fill in what I am doing as I have not got the energy to even find a pen. Each month I would turn up and for over a week after attending I was ill from pain and exhaustion. However, still undeterred, I made it for the whole year's sessions leaving out one as I was too ill to go. October 2005, they ended the monthly get togethers and told us we would be emailed re. our next session. October 2006, we were now down to five persons and were asked how we felt the CBT had helped. And that this was the last appointment; the look on the four people with me was one of astonishment and questions like - is that it, no follow-up? We left in utter dismay; we had seen no consultants; nothing was ever done for us medically, just flip charts and forms. In one of the sessions a man collapsed we were afraid for him because most of us knew that when a person collapses with ME he needs to be laid down and cared for; as he fell forward in his chair, the group leader said leave him, he will be ok; there was no compassion for this man. Conclusion: ... The whole exercise was a waste of NHS money as we were all long term sufferers who had learnt to PACE, through trial and error. For the people who suffered ME pain there was no help; we were told that for our pain it would be better if we steer clear of certain kinds of pain killers that were likely to help, as they were mainly morphine based and we would end up having addictive problems. Extracts from RiME Newsletter, Autumn 2005: Kathleen McCall, leader of the Winchester and Eastleigh ME Group: ... What makes me laugh is that to our face they call this the ME/CFS Clinic when in reality it's the Hants and IOW Chronic Fatigue Service.... We are meant to be reassured by the fact that the Southampton Clinic is modelled on the Wareham Clinic in Dorset. From correspondence I've received from PWME who've attended the Wareham Clinic, I'm not reassured at all, as Wareham seems to show a strong psychiatric bias of it's own. One ME patient at Wareham was told she was having treatment based on physical strategies for dealing with ME; they then wrote to her GP saying treatment was focused on 'identifying and challenging negative thought processes that could have hindered her recovery... ' What PWME primarily want is proper research into their condition and, with this mind, we support RiME's efforts... '' ... Chair of Birmingham Solihull Group, 13/7/05: The members wish to express their deep concern that the patients' representatives... are clearly being excluded form any meaningful dialogue in the development of the new services for ME/CFS at the Birmingham and West Midlands CNCC and the S Birmingham LMDT. Assurances were given that, although the Birmingham + Solihull Mental Health trust was chosen to 'site' the bid, the new ME/CFS services would operate independently from the psychiatric service. This is not the case.... Accordingly Solihull and S Birmingham Support group have advised their patient representatives to disengage from any further participation... The latter, 11/2/07: I see West Midlands CNCC going the same way as many others - very short of funding and not much on offer in the way of anything except diagnosis. Our members' view is mostly the same as your contacts - nothing in it for them and certainly not what they wanted. We asked the members who had been to the clinic to rate it out of five and we had a lot of zeros. <rimexx tiscali.co.uk> www.erythos.com/RiME [Return to top] ------------------------------ Date: Fri, 13 Jul 2007 11:33:48 -0400 From: "Bernice A. Melsky" <bernice.melsky1 VERIZON.NET> Subject: RES: Increased Levels of Neurotrophins Are Not Specific for Chronic Migraine: Evidence from Primary Fibromyalgia Syndrome Increased Levels of Neurotrophins Are Not Specific for Chronic Migraine: Evidence from Primary Fibromyalgia Syndrome. J Pain. 2007 Jul 3; [Epub ahead of print] Sarchielli P, Mancini ML, Floridi A, Coppola F, Rossi C, Nardi K, Acciarresi M, Alberto Pini L, Calabresi P. Neurologic Clinic, Department of Medical and Surgical Specialties and Public Health, University of Perugia, Perugia, Italy. PMID: 17611164 All data obtained in experimental animal pain models support the role of nerve growth factor (NGF) as a putative candidate intervening in the pathogenesis of chronic pain, including chronic daily headache (CDH). Few studies have been carried out to establish its role in maintaining pain states in humans. The present study was aimed at investigating cerebrospinal fluid (CSF) levels of NGF and brain-derived neurotrophic factor (BDNF), both measured by sensitive immunoassay, in 20 chronic migraine (CM) patients and 20 patients affected by primary fibromyalgia syndrome (PFMS), compared with those of 20 age-matched control subjects. Significantly higher levels of both neurotrophins and glutamate were found. A significantly positive correlation emerged between CSF values of BDNF and those of NGF (r = .61, P < .001; r = .53, P < .01) and glutamate (r = .44, P < .02; r = .51, P < .01) in CM and PFMS patients, respectively. These findings suggest the possibility of a NGF-mediated up-regulation of BDNF involved in the pathophysiological events underlying long-term neuroplastic changes in persistent chronic painful conditions, such as CM and fibromyalgia. NGF might indirectly exert its effect through enhancing glutamatergic transmission via BDNF. The above mechanisms could account for sustained central sensitization in both chronic pain states. PERSPECTIVE: This article presents findings of higher NGF and BDNF levels correlated to increased glutamate levels in the CSF of both chronic migraine and fibromyalgia patients. This opens new insights into the pathogenic mechanisms of chronic pain and offers clinicians new therapeutic perspectives targeting the above mechanisms in both painful disorders. [Return to top] ------------------------------ Date: Fri, 13 Jul 2007 19:18:07 +0200 From: "Dr. Marc-Alexander Fluks" <fluks@COMBIDOM.COM> Subject: RES,NOT: CDC sponsors CFS photo exhibit Source: CNHI News Service Date: July 13, 2007 Author: Julie Kirkwood URL: http://www.eagletribune.com/pulife/local_story_194093857?keyword=topstory Fighting fatigue: Local woman, art show work to battle stigma of chronic fatigue syndrome ------------------------------------------------------------------------ Jean Harrison knows that some of her former colleagues in the art world think she was a prima donna, or worse, that she was lazy. Toward the end of her career restoring paintings, she was working at the Peabody Essex Museum in Salem, Mass., and had days when she couldn't get herself out of bed before 1 p.m. She often worked at the museum alone until 11 p.m. or later eating Cheez-It crackers and drinking Diet Coke. Her work sometimes wasn't finished until the very last minute. Some days, she slept 16 or 18 hours. Thinking it might be depression, she saw a doctor. She took kung fu classes, hoping exercise would help. She even got tested for attention deficit disorder. "I was eager to find anything that would treat this," Harrison said. "I knew there was something wrong." Nothing worked. She got worse. "I went to the museum one day and said I thought I would probably be out of work for a while," Harrison said. "I was crawling on the floor - crawling, literally - to get to the bathroom... I was probably asleep almost 20 hours a day, easily." That was in 1994. Harrison, 54, now knows she has chronic fatigue syndrome, a disease that affects an estimated 1 million Americans, the majority of whom have never been diagnosed. It is a disease that many people assume is all in the patient's head, even though numerous research articles have been published showing otherwise, said Kim McCleary, president and chief executive officer of a patient advocacy group called The Chronic Fatigue and Immune Dysfunction Syndrome Association of America. That's why The CFIDS Association has put together a photo exhibit, funded by the federal Centers for Disease Control and Prevention, of people who have chronic fatigue syndrome. It opens at the Boston Public Library on Monday, July 16. "We chose people who might, as a group, represent people you'd see in the mall or the library, people who would remind you of all the people in your life that could have this," McCleary said. The purpose is to help the roughly 80 percent of patients who don't know they have the disease to learn about chronic fatigue syndrome and feel comfortable seeking help, she said. "This is real and it has a devastating effect on people's lives," McCleary said. "But there's hope out there. There's courage and dignity, even though there is still some stigma." Harrison believes her chronic fatigue symptoms started when she was only 6 years old, and have reoccurred periodically throughout her life. She was lethargic through most of her childhood, but she got good grades and breezed through Wellesley College, she said, earning an art history degree. Then she had a bad episode several years later when she was in England learning art restoration. She felt ill and her glands were so swollen, she said her doctor thought she had lymphoma. This was in the 1980s, a few years before the phrase "chronic fatigue syndrome" was coined and made a big splash in the American media. What brought it to the public's attention were two cluster outbreaks of the symptoms, McCleary said, and the scientists looking for the cause quickly discovered other patients who weren't associated with the clusters. The stigma followed close behind, as patients - often Caucasian, upper-middle-class women who could afford to push for answers - went to their doctors complaining of symptoms that couldn't be confirmed by any laboratory test. "The term 'yuppie flu' came into use," McCleary said. "That was a real misnomer but it stuck. Then it sort of developed into this perception that these were just whiny, white women - type A personalities - who said 'I want it all,' then decided they didn't want it all anymore and this was their way out... Medical providers just sort of wrote these people off as having a character weakness or something. It really did create a barrier to medical care." Harrison was fortunate enough to find a doctor who took her condition seriously and supported her, even when she wanted to try an experimental new treatment. Harrison had read studies showing that some chronic fatigue syndrome patients have low blood volume, so she went to Salem (Mass.) Hospital to get tested. Sure enough, her blood volume was low. Her doctor supported her decision to try something experimental: regular infusions of saline solution directly into her bloodstream. Initially the infusions were given through her arms, but she now has a Port-A-Cath surgically implanted in her chest. She gives herself infusions several times a week. Though the infusions made her feel much better, she said chronic fatigue is still something she fights every day. In some ways it's harder now, she said, because she looks healthy. "I'm not missing an arm," Harrison said. "I'm not missing a leg. I look fine." As a result, people don't understand why she avoids even the lightest physical exertion, which she has learned through experience will make her exhausted for days. Even her own family looks at her with skepticism when she suddenly has to lie on the floor because her blood pressure has dropped, even though "orthostatic instability" (instability when standing) is a well-documented side effect of chronic fatigue syndrome. When Harrison stands up, her blood pressure drops, her pulse races, she feels dizzy and her brain goes haywire. If she stands up in the middle of a telephone conversation, she said, she loses her train of thought. "I'm not stupid," she said. "It's just there's something neurologically wrong." Harrison said she hesitated about telling her story because some people still don't take the disease seriously. She said she knows other people living North of Boston who have chronic fatigue syndrome but don't tell anybody because they don't want to lose credibility. Instead, she said, they say they have a back problem, or make up some other excuse to lie down. What made her decide to tell her story is the same thing that McCleary believes motivated patients to have their portrait taken for the chronic fatigue photo exhibit. "It's so important that the message get out, how devastating this can be," Harrison said. If you go * What: "The Faces of Chronic Fatigue Syndrome" photo exhibit, part of a $6 million public awareness campaign funded by the U.S. Centers for Disease Control and Prevention * Where: Boston Public Library, 700 Boylston St., Boston * When: Monday, July 16, through Monday, July 23 * How: Admission is free. For more, call 800-442-3437 or check out http://www.cfids.org. -------- (c) 2007 Community Newspaper Holdings, Inc. [Return to top] ------------------------------ Date: Fri, 13 Jul 2007 20:54:33 -0400 From: "LK Woodruff <lkw777 charter.net> [via Co-Cure Moderators] Subject: MED: ME - Tests which can aid diagnosis ***PERMISSION TO REPOST*** ME: Tests which can aid diagnosis include: SPECT and xenon SPECT scans of the brain SPECT scans have demonstrated decreased cerebral blood flow most frequently in the frontal, parietal, temporal, occipital and brain stem areas of the brain. This decrease in cerebral blood flow has also found to be worsened further still 24 - 48 hours post-exertion. These abnormalities have also been shown to correlate with clinical status. (Carruthers et al. 2003) Dr Byron Hyde MD adds that, 'I do not describe a patient as having M.E. unless there is an abnormal SPECT. If the SPECT is normal, I often repeat it along with xenon SPECT. If the brain scans remain normal, I conclude that it is unlikely to be M.E.' (Hyde, 2003) MRI scans of the brain MRI scans have shown the presence of small white matter lesions predominantly in the frontal lobes. Punctate, subcortical areas of high signal intensity consistent with edema or demyelination were identified by MRI in 78% of M.E. patients (similar to those seen in MS). The abnormalities in M.E. patients most closely resemble those seen in AIDS encephalopathy. Research has shown that an estimated 80% of M.E. patients will have abnormal MRI scans. (Hyde, 2003) (Carruthers et al. 2003) M.E. patients with abnormalities on MRI have been reported as being more severely impaired than those without such abnormalities. In a comparison of intracranial abnormalities in M.E. patients by MRI and SPECT, the SPECT scan abnormalities appeared to correlate with clinical status while the MRI changes were irreversible. (Carruthers et al. 2003) MRI scans are also not recommended however for those patients which relapse when exposed to loud noises (a common symptom of M.E.); an MRI scan can cause severe and extended relapse in such patients. Dr Byron Hyde MD also explains that a normal MRI does not conclusively prove that a person has no CNS dysfunction as the MRI demonstrates only abnormal anatomy and so a normal MRI should never be used to prove that a person does not have CNS dysfunction or is not ill. (2003) PET scans of the brain PET scans have shown decreased metabolism of glucose in the right mediofrontal cortex. PET scans have also shown generalised hypoperfusion of the brain with a particular pattern of decreased neuronal metabolism in the brain stem. (Carruthers et al. 2003) (CT scans however are not appropriate or useful for diagnosing M.E. or for investigating M.E. pathology. Most M.E. patients will have a normal CT scan.) Neuropsychological testing Of the CNS dysfunctions that make up M.E., cognitive dysfunction is easily one of the most disabling characteristics of the illness. The cognitive dysfunction in M.E. can be extremely severe. (Hyde, 1992) Neuropsychological testing can be used to identify cognitive dysfunction and/or to confirm a M.E. diagnosis. It should focus on the abnormalities known to differentiate M.E. from other causes of organic brain dysfunctions. (Carruthers et al. 2003) Dr Sheila Bastien PhD. is easily the expert in this field with over 20 years experience in neuropsychological testing and more than 6 years experience in applying these tests to M.E. patients. She explains that: Deterioration of IQ levels, as well as cognitive and motor dysfunction in these patients, suggest a pathological process in the brain. The pattern of focal and lateral impairments is consistent with patients who have this particular neurologic dysfunction. The impairment pattern is consistent across the study group [of M.E. patients] although impairment levels vary. This pattern is not seen in other diseases or injuries, such as Alzheimers, stroke, head injuries, multiple sclerosis, systemic lupus erythematosis, personality disorders, depression, psychosis, malingering, anxiety or panic disorders, somatisation or situational stress disorders. The pattern of impairment is one of focal and lateral deficits, consistent with a multi-focal organic brain syndrome. Tests suggest that the most impaired focal areas are the left temporal, right paretal, and left temporal lobes; although there are lesser bilateral impairments in the opposite lobes as well. (1992, pp. 453 - 454) Dr Byron Hyde MD adds that: 'This is a complex type of testing, and a physician should attempt to locate an experienced neuropsychologist without ties to the insurance industry. Most neuropsychologists today are employed by the insurance industry, and if they find too much pathology, I suspect that they are no longer engaged. Do not be fooled by a negative insurance-paid neuropsychological report; psychologists whose primary training is not neuropsychology prepare many of these reports.' (2003) One of the most useful texts on neuropsychological testing in M.E. is chapter 51 of the book 'The Clinical and Scientific Basis of ME' written by Dr Sheila Bastien Ph.D. Several other chapters of this book also describe the various cognitive effects of M.E. in detail. (Details of this book are given below.) See also The Ultra-comprehensive Myalgic Encephalomyelitis Symptom List for more information about the specific cognitive deficits commonly seen in M.E. EEG brain maps and QEEG brain maps 95% of M.E. patients have been found to have abnormal cognitive-evoked EEG brain maps (Hooper, 2001 [Online]). But Dr Byron Hyde MD argues that QEEG brain maps are even more accurate: An EEG only records activity on the outer millimeter of the brain. A QEEG is simply an EEG attached to a computer that contains appropriate software. A QEEG will immediately demonstrate tumors and brain activity or lack of it related to specific stimuli that are simply not possible to detect on a non-computer-driven EEG. Using QEEG technology operated by an expert physician, we have been able to demonstrate not only lack of normal activity in ME patients but migration of the normal activity centers from injured areas to different parts of the brain. (Hyde, 2003) Romberg or tandem Romberg test The test involves standing with eyes open and then with eyes closed with feet together or one behind the other. A positive Romberg is when the position is maintained with eyes open but not when they are closed. It is a useful test of brain stem function. Professor Malcolm Hooper explains that, 'In his 1995 Australian Workshop, M.E. expert Dr Paul Cheney said that more than 90% of patients have an abnormal Romberg versus 0% of controls.' (Hooper et al. 2001 [Online.]) Neurological examination Most M.E. patients have abnormal neurological examination. (Hooper et al. 2001 [Online.]) Tests of the immune system The immune system abnormalities in M.E. patients mimic the immune pattern seen in viral infections. Specific findings include (but are not limited to): Increased numbers of activated cytotoxic T cells (most patients have evidence of T-cell activation) Low natural killer cell numbers/percentage and function (cytotoxicity) Elevated immune complexes Atypical lymphocyte count Significantly reduced CD8 suppressor cell population and increased activation marker (CD38, HLA-DR) on CD8 cells Abnormal CD4/CD8 ratio Elevations of circulating cytokines Immunoglobulin deficiencies (most often IgG 1 and IgG 3) (McLaughlin, 2004 [Online]) (Carruthers et al. 2003) (Hooper et al. 2001 [Online.]) One doctor commented (in a presentation on the immunological markers in M.E.) that: The NK (natural killer) cell is a very critical cell in [M.E. equivalent] CFS because it is clearly negatively impacted. The most compelling finding was that the NK cell cytotoxicity in CFS was as low as we have ever seen it in any disease. This is very, very significant data. [In CFS] the actual function was very, very low -- 9% cytotoxicity: the mean for the controls was 25, In early HIV and even well into ARC (AIDS related complex, which often precedes the fully developed condition), NK cytotoxicity might be around 13 or 14 percent. (ME)CFS patients represent the lowest cytotoxicity of all populations we've studied. (Klimas, 1990) Professor Malcolm Hooper adds that: 'There is mounting international evidence that M.E. is an autoimmune disorder, with similarities to systemic lupus erythematosus. Evidence of antilamin antibodies has been found in the blood of M.E. patients: antibodies against this protein are proof of autoimmunity and of damage to brain cells.' (2001 [Online.]) RNase L A more specific immune system abnormality has been discovered in ICD-CFS of increased activity and dysfunction of the 2-5A RNase-L antiviral pathway in lymphocytes. The dysregulation of the RNase-L pathway strongly supports the hypothesis that viral infection plays a role in the pathogenesis of the illness. Between 80 - 94.7% of M.E. patients have evidence of an up-regulated 2-5A antiviral pathway; are so positive for this marker. The degree of elevation of 37 kDa Rnase L has also been shown to correlate with symptom severity. This test is as yet not widely available but may be one of the most useful tests in helping to diagnose ICD-CFS in the future. (See Red Labs for more information.) (Carruthers et al. 2003) Erythrocyte Sedimentation Rate (ESR) An unusually low sedimentation rate of less than 5mm/hr is common in M.E. (although there may also be brief periods where there is an elevated rate >20mm/hr). (Hooper et al. 2001 [Online.]) ESR rates as low as 0 have been documented in M.E. patients. Insulin Levels and Glucose Tolerance Tests Derangement of insulin response and insulin levels is a frequent finding in M.E. patients. Glucose tolerance curves are often abnormal. (Hooper et al. 2001 [Online.]) 24 Hour Holter Monitor A 24 hour Holter monitor (a type of heart monitor) may show repetitively oscillating T-wave inversions and/or a flat T-wave may be found. (A standard 12 lead ECG is usually normal however.) (Hooper et al. 2001 [Online.]) Holter monitors may also show heart rates as high as (or higher than) 150 beats per minute as an immediate or delayed response to the patient maintaining an upright posture, or at rest. (Carruthers et al. 2003) Heart rates as low as 40 beats per minute may also be observed (during sleep). (Hyde, 2003) Dr Byron Hyde MD explains that: I routinely use a Holter monitor on all patients. The cardiologist often reports these as normal. Do not trust this report. What the cardiologist or computer is basing the report on is the number of ischemic events [which is not relevant to the heart problems caused by M.E.]. However, read the lowest heart rate at night, and note that it sometimes falls to the low 40's. Though this may be normal in an athlete, it is not in a sedentary M.E. patient. For a patient who is not active all day long and has an average heart rate that flirts with 100 beats per minute or more, you know that this is not normal. These abnormal tests, however, are often reported as normal.' (Hyde, 2003) Dr Byron Hyde MD and the Canadian Guidelines both recommend that patients or doctors must always specifically request to be informed of these specific patterns as they may not be reported (or may be subsumed under non-specific T-wave changes) by the interpreter. (Hyde, 2003) (Carruthers et al. 2003) Tilt Table Examination The Canadian Guidelines explain that: Investigation by tilt test is indicated if there is a fall in blood pressure and/or excessive rapidity of heart beat upon standing, which improves when sitting or lying down. Patients often report that they experience dizziness, feeling light-headed or 'woozy' upon standing, or feeling faint when they stand up or are standing motionless such as in a store checkout line. Patients may exhibit pallor and mottling of the extremities. These historical symptoms and signs are sufficient for the initial diagnosis. As [M.E.] patients often have a delayed form of orthostatic intolerance, taking the blood pressure after standing may not be effective in diagnosis. Rather than having the patient stand for a period of time where there is a risk of him/her falling, we recommend using the tilt test where the patient is strapped down. The tilt test involves the patient lying horizontally on a table and then tilting the table upright to a 60°-70° angle for appproximately 45 minutes during which time blood pressure and heart rate are monitored.' (2003) Orthostatic intolerance is very common in M.E. patients and may manifest as one of, or a combination of the following: Neurally mediated hypotension (NMH): Involves disturbances in the autonomic regulation of blood pressure and pulse. There is a precipitous drop that would be greater than 20-25 mm of mercury of systolic blood pressure upon standing, or standing motionless, with significant accompanying symptoms. The patient feels an urgency to lie down. Postural orthostatic tachycardia syndrome (POTS): Excessive rapidity in the action of the heart (either an increase of over 30 beats per minute or greater than 120 beats per minute during 10 minutes of standing); and a fall in blood pressure occurring upon standing. Syncope can but usually does not occur. Delayed postural hypotension: As above except the drop in blood pressure occurs many minutes (usually ten or more) after the patient stands rather than upon standing. (Carruthers et al. 2003) (Bassett 2005, [Online]) ******************************************************** WARNING! Dr Byron Hyde MD warns about tilt table testing in M.E. patients however that: I frequently find gross abnormalities in M.E. patients with this test. [But] a circulating blood volume and a complete cardiac investigation should be done first. This is not a test to undertake lightly since the patient's heart sometimes stops and may have to be restarted. This test should only be done in major hospital centers in the presence of an appropriate physician where such emergency capabilities can be instituted.' (Hyde, 2003) ******************************************************** Exercise testing and chemical stress tests Cardiopulmonary exercise testing (CPX) is widely used for the diagnosis (and functional assessment) of various cardiac and metabolic disorders and can also be used in the diagnostic evaluation of M.E. patients. Heart rate and blood pressure responses during the exercise test may reveal abnormalities specific to ME including: lower cardiovascular and ventilatory values at peak exercise (patients only being able to attain half the expected maximal workload and oxygen uptake compared to sedentary controls), elevated resting heart rates and an inability to reach maximum age-predicted heart rates (suggesting cardiac or peripheral insufficiency and/or reduced blood volume). (Carruthers et al. 2003) Many more severely affected M.E. patients however will be either too ill to complete such tests altogether, or may be able to complete these tests only at the cost of a potentially severe and unnecessary relapse (which usually peaks 24 - 48 hours post-exercise and will then persist for days, weeks or even months afterward depending on the patient's illness level). In addition to the risk of relapse, there have also been reports of sudden deaths in M.E. patients following exercise as M.E. expert Dr Elizabeth Dowsett explains: 'Some 20% [of M.E. patients] have progressive and frequently undiagnosed degeneration of cardiac muscle which has led, in several cases, to sudden death following exercise.' (2000 [Online]) As exercise tests are not appropriate for many M.E. sufferers, Dr Byron Hyde MD writes: Patients with ME frequently cannot do exercise tests, and so I then do chemical testing as a second best. Several of our patients have reacted severely to the chemical test with excruciating pain. This is not true angina, and although the pain sometimes ceases as soon as the chemical is stopped and the antidote given, sometimes it persists for weeks after the procedure with no sign of coronary artery disease. I do not understand this phenomenon, but it is obviously vascular. The cardiologists state that this pain does not occur with the same frequency in non-ME patients. (2003) Miscellaneous other abnormalities commonly found in M.E. patients: Cholesterol (high), cortisol (low), thyroid stimulating hormone (TSH) (low), potassium (low), prolactin (high). Physical Exam There are also abnormalities visible on physical exam in M.E. patients. These abnormalities are not usual in healthy patients but they are also found in people with other illnesses (so they are not specific to M.E.). In cases of severe or acute M.E. there are always definite physical signs indicative of physical illness but virtually all patients will have some abnormality on physical exam. Not all patients will have all signs and along with a fluctuating course of the illness from hour to hour and from day to day being one of the key characteristics of M.E., signs of the illness may also change or fluctuate during the course of a day. As M.E. expert Professor Malcolm Hooper explains: 'a patient examined in the morning might have nystagmus, which would disappear at midday, recur later, disappear and recur the next day; thus a once-only cursory examination could be misleading.' (Hooper et al. 2001 [Online.]) Physical signs of illness commonly observed in M.E. patients include: Nystagmus; nystagmus is jelly-like and variable (15% of M.E. patients will have nystagmus) Sluggish visual accommodation Unequal pupils and contrary pupil reaction to light A labile blood pressure (sometimes as low as 84/48 in an adult at rest) Shortness of breath (particularly on exertion) Sometimes marked falling pulse pressure in arterial pressures taken first when prone, then sitting, then standing Rapid heart rate on minor activity such as standing Subnormal temperature Patients show significant reduction in all lung function parameters tested Liver involvement (an enlarged liver or spleen) Abnormal tandem or augmented tandem stance Abnormal gait Hand tremor Incoordination Cogwheel movement of the leg on testing Muscular twitching or fasciculation Hyper-reflexia without clonus Facial vasculoid rash Vascular demarcation which can cross dermatomes with evidence of Raynaud's syndrome and / or vasculitis and spontaneous periarticular bleeds in the digits Mouth ulcers Hair loss Destruction of fingerprints is sometimes seen (atrophy of fingerprints is due to perilymphocytic vasculitis and vacuolisation of fibroblasts) Ghastly pallor of face with frequent lupus-like submaxillary mask Parkinsonian rigidity of facial expression Scanning, disjointed speech, or speech reversals Nasal passage obstruction and inflamed areas around tonsillar pillars Sicca syndrome of conjunctiva and mucous membranes Frequent equivocal Babinski/plantar reflex on one side Unusual sensitivity of cervical vertebrae area Nodular thyroid (Hooper et al. 2001 [Online.]) (Hyde, 2003) In addition, the diagnosis of M.E. should never be made without the post-exertional paralytic muscle weakness which is unique to M.E. being present. M.E. authority Dr Melvin Ramsay explains that this unique symptom: 'is virtually a sheet-anchor in the diagnosis of Myalgic Encephalomyelitis and without it a diagnosis should not be made.' Muscles may function normally to begin with but there is a continued loss of post-exertional muscle power after even a minor degree of physical effort; three, four or five days, or longer, elapse before full muscle power is restored. ([Online]) (In sedentary controls full muscle power is restored after just 200 minutes.) All muscles are affected, including the heart. (Hooper et al. 2001 [Online.]) Thus a patient may be easily able to lift/push/squeeze something with close to normal strength several times, or for a short period; but be unable to complete the same task (or even a trivial task) repeatedly (such as lifting a soup spoon many times for example). Professor Malcolm Hooper recommends testing for this by observing the patient repeatedly lifting something weighing around 2 pounds for a period of time. He explains that, 'M.E. patients can often manage a small number of repeats but performance rapidly falls off and recovery is very slow compared to healthy controls. More sophisticated treadmill tests will also show the same effect.' This sudden onset muscle weakness (or paralysis) and very slow recovery is uniquely characteristic of M.E. patients. (2003). SOURCE: http://www.ahummingbirdsguide.com:80/testingforme.htm by Jodi Basset [Return to top] ------------------------------ Date: Sat, 14 Jul 2007 13:58:16 +0200 From: "Dr. Marc-Alexander Fluks" <fluks@COMBIDOM.COM> Subject: RES,NOT: Brown & Jason study on CFS, FM, and MCS Source: American Chronicle Date: July 13, 2007 Author: Lourdes Salvador URL: http://www.americanchronicle.com/articles/viewArticle.asp?articleID=31056 The Effect of Illness Accumulation on Quality of Life ----------------------------------------------------- It would seem obvious to most people that the more illnesses one has, the less functional they would be. Scientists, on the other hand, must prove things via empirical studies. In a study titled Functioning in individuals with chronic fatigue syndrome: increased impairment with co-occurring multiple chemical sensitivity and fibromyalgia, Brown and Jason (2007) set out to "differentiate these diagnoses by comparing individuals with one or more illnesses on functioning, psychiatric comorbidity, coping style, and in vivo physical measures". Brown and Jason were spurred by the proposal that chronic fatigue syndrome (CFS), multiple chemical sensitivity (MCS), and fibromyalgia (FM) commonly co-occur and may be manifestations of the same illness. The researchers surveyed 114 men and women who met the criteria for CFS. They further diagnosed FM during a physical examination, and MCS using a questionnaire. The men and women were then divided into four groups based on diagnoses: 43.9% met criteria for CFS, 23.7% met criteria for CFS & MCS, 15.8% met criteria for CFS & FM, 16.7% met criteria for all three. Demographics varied widely. A total of 46% were referred by physicians, 34% from media advertisements, and 20% from word-of-mouth. After an initial screening, participants were given a CFS questionnaire to collect demographics, health status, medication usage, and symptom data. This was followed by a structured clinical interview for DSM-IV (Diagnostic and Statistics Manual of Mental Disorders) disorders to determine presence of any mental disorders. A medical assessment of CFS was performed, including an in-depth medical and neurological history, and physical exam. A self-report measure was used for general functioning. The Fatigue Severity Scale was added to measure fatigue and the Beck Depression Inventory was included to measure depression. A Brief Cope and Brief Pain was administered to determine how subjects reacted to stress and pain respectively. An Actiograph, designed to measure activity during every minute of a week was worn to record daily activities. A six minute walking test measured physical functioning and the Rating of Perceived Exertion was used to measure subjects perception of the intensity of their activity based on bodily sensations. Sit and reach, hand grip, and employment status were the final factors examined that concluded this extensive battery of measures. As you undoubtedly guessed, the more conditions the subject had, the more impaired they were. Those with CFS alone were the highest functioning and those with CFS, FM, and MCS were the lowest functioning, leading Brown and Jason to conclude that "this study provides evidence that having more than one illness exacerbates one's disability beyond CFS alone", which we have already guessed would be the case. No significant differences were found in varying socio-demographic categories. A rather large percent of subjects (68%) had a college degree or higher, suggestive of prior functioning. A substantial number of CFS patients (56%) had co-occurring MCS and/or FM, which is consistent with prior study findings that have shown significant overlap between MCS, CFS, and FM. Depression was more common in those with MCS, CFS, and FM combined, suggesting increased prevalence of depression in those who are more severely disabled. Overall, this exhaustive study has shown that increased disability means decreased functioning. It is important to remember that all participants in this study suffered from CFS. FM and MCS was not evaluated alone or as a pair without the presence of CFS. Reference Brown, MM & and Jason, LA (2007). Functioning in individuals with chronic fatigue syndrome: increased impairment with co-occurring multiple chemical sensitivity and fibromyalgia. Dynamic Medicine 2007, 6:6 -------- (c) 2007 American Chronicle [Return to top] ------------------------------ Date: Sat, 14 Jul 2007 19:44:32 -0400 From: "Bernice A. Melsky" <bernice.melsky1 VERIZON.NET> Subject: RES: Paraoxonase and arylesterase activities in fibromyalgia Paraoxonase and arylesterase activities in fibromyalgia. Redox Rep. 2007;12(3):134-8. Altindag O, Gur A, Calgan N, Soran N, Celik H, Selek S. Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Harran University, Sanliurfa, Turkey. ozaltindag yahoo.com PMID: 17623520 We aimed to evaluate the association of serum paraoxonase and arylesterase activities and oxidative/antioxidative status in patients with fibromyalgia. Forty-two patients with fibromyalgia and 53 healthy controls were included in the study. Serum paraoxonase and arylesterase activities were measured spectrophotometrically. Oxidative and antioxidative status were evaluated by measuring serum lipid hydroperoxide (LOOH) levels, total antioxidant status (TAS) and free sulfhydryl groups (-SH = total thiol). Lipid parameters were determined by routine laboratory methods. Serum paraoxonase and arylesterase activities, and TAS were lower in patients with fibromyalgia than in controls (P < 0.001, for all), and the -SH level was also lower in the patient group (P = 0.03). LOOH levels were higher in the patient group than in controls (P = 0.01). Our results suggest that patients with fibromyalgia were exposed to oxidative stress, and paraoxonase and arylesterase activities were decreased in these patients. Patients with fibromyalgia might be prone to development of atherosclerosis with reduced paraoxonase and arylesterase activities. [Return to top] ------------------------------ Date: Sun, 15 Jul 2007 12:30:51 -0400 From: "Bernice A. Melsky" <bernice.melsky1 VERIZON.NET> Subject: RES: The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation Medical Hypotheses, Volume 69, Issue 3, 2007, Pages 517-525 David L. Katz [a, b, *], Lindsey Greene [a], Ather Ali [a, b] and Zubaida Faridi [a] [a] Yale Prevention Research Center, Yale University School of Medicine, 130 Division Street, Derby, CT 06418, USA [b] Yale University School of Public Health, Yale University School of Medicine, 60 College Street, New Haven, CT 06520, USA [*] Corresponding Author. Present address: Yale Prevention Research Center, 130 Division Street, Derby, CT 06418, USA. Tel.: +1 203 732 1265; fax: +1 203 732 1264. Received 12 October 2005; accepted 16 October 2005. Available online 28 March 2007. Summary Fibromyalgia syndrome (FMS) is a condition of chronic muscle pain and fatigue of unknown etiology and pathogenesis. There is limited support for the various hypotheses espoused to account for the manifestations of FMS, including immunogenic, endocrine, and neurological mechanisms. Treatment, partially effective at best, is directed toward symptomatic relief without the benefit of targeting known, underlying pathology. A noteworthy commonality among partially effective therapies is a vasodilatory effect. This is true both of conventional treatments, unconventional treatments such as intravenous micronutrient therapy, and lifestyle treatments, specifically graduated exercise. The pain of fibromyalgia is described in terms suggestive of the pain in muscles following extreme exertion and anaerobic metabolism. Taken together, these characteristics suggest that the pain could be induced by vasomotor dysregulation, and vasoconstriction in muscle, leading to low-level ischemia and its metabolic sequelae. Vasodilatory influences, including physical activity, relieve the pain of FMS by increasing muscle perfusion. There are some preliminary data consistent with this hypothesis, and nothing known about FMS that refutes it. The hypothesis that the downstream cause of FMS symptoms is muscle hypoperfusion due to regional vasomotor dysregulation has clear implications for treatment; is testable with current technology; and should be investigated. Copyright © 2007 Elsevier Ltd All rights reserved. [Return to top] ------------------------------ Date: Mon, 16 Jul 2007 11:40:50 -0400 From: "Bernice A. Melsky" <bernice.melsky1 VERIZON.NET> Subject: RES: Dysautonomia, fibromyalgia and reflex dystrophy Dysautonomia, fibromyalgia and reflex dystrophy. Arthritis Res Ther. 2007 Jul 6;9(4):105 [Epub ahead of print] Eisinger J. Unit Infomyalgies, Centre Hospitalier, 83056 Toulon, France. <email@example.com>. PMID: 17626612 ABSTRACT: Autonomic nervous system dysfunction observed in fibromyalgia, characterized without exception by a sympathetic hyperactivity and hyporeactivity, has been reported. However, several studies demonstrated reduced levels of norepinephrine and neuropeptide Y at rest and after tilt table in some patients, which was improved by beta-stimulating agents. These findings support heterogeneity in fibromyalgia-associated dysautonomia. Fibromyalgia could be a generalized sympathetic dystrophy since both conditions are activated by trauma and partly linked to sympathetic mechanisms. Yet they differ on several points: hormonal and neurochemical abnormalities are observed in fibromyalgia whereas activation by peripheral trauma and hyperosteolysis are observed in reflex sympathetic dystrophy. 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