pacmanx1

I tried to post earlier but something happened to it and it just disappeared. What are your service connected conditions? I do not have CFS, but I do have fibromyalgia with fatigue. Some people that have CFS also have fibromyalgia and they can be rated separately. People with CFS also have IBS and that can be rated separately also. Hope this Helps http://chronicfatigu...inked/a/IBS.htm

I agree with Carlie, all is not lost. I found this on-line and it has been wrecking my mind for months. How did you file your claim? When was your CUE filed again? Change Date December 29, 2007 a. Definition: Clear and Unmistakable Error A clear and unmistakable error (CUE) is an error that is undebatable in that a reasonable mind can only conclude that the original decision was fatally flawed at the time it was made. b. Provisions of 38 CFR 3.105(a) 38 CFR 3.105(a) provides that if clear and unmistakable error is established in a previous rating determination, then the · prior decision is reversed or amended, and · effect is the same as if the corrected decision had been made on the date of the reversed decision. 7. Clear and Unmistakable Error (CUE), Continued c. Determination Requirements A CUE determination must be based on the record and the law that existed at the time of the prior decision. In a valid claim of CUE, the claimant must assert more than a disagreement as to how the facts were weighed or evaluated. There must have been an error in prior adjudication of the claim. Example: A new medical diagnosis that corrects an earlier diagnosis ruled in a previous rating would not be considered an error in the previous adjudication of the claim. d. Identifying a CUE A CUE exists if · there is an error that is undebatable so that it can be said that reasonable minds could only conclude that the previous decision was fatally flawed at the time it was made · Department of Veterans Affairs (VA) failed to follow a procedural directive that involved a substantive rule · VA overlooked material facts of record, or · VA failed to apply or incorrectly applied the appropriate laws or regulations. Note: If the claimant contends that VA's failure to follow a procedural directive determined the outcome of the claim, contact the Compensation and Pension (C&P) Service for advice on any rule-making arguments that may have been advanced. References: For more information on · CUE, see 38 CFR 3.105(a) · potential errors in following procedures, see Allin v. Brown, 6 Vet. App. 207 (1994), and · CUEs based on VA's constructive notice of medical records, see - VAOPGCPREC 12-95, and - M21-1MR, Part III, Subpart iv, 1.3. <BR style="mso-special-character: line-break"><BR style="mso-special-character: line-break">

A Review of Chronic Fatigue(ME/NDS) August 22, 2010 posted by Denise Nichols A Review of CFS as it stands at this time. Hopefully news of the XMRV or the new name possibily a human infectious gamma retrovirus – the first one we know of an HGRV….. will be published this week and maybe we will see rapid developments in the field and an expedited time table to finally get to the answers that at least a million people have been waiting for years. Thanks to the civilian side of the House this is what we know so far, although this is the basics for review purpose. What is Chronic Fatigue Syndrome? We all get tired. Many of us at times have felt depressed. But the mystery known as chronic fatigue syndrome (CFS) is not like the normal ups and downs we experience in everyday life. The early sign of this illness is a strong and noticeable fatigue that comes on suddenly and often comes and goes or never stops. You feel too tired to do normal activities or are easily exhausted with no apparent reason. Unlike the mind fog of a serious hangover, to which researchers have compared CFS, the profound weakness of CFS does not go away with a few good nights of sleep. Instead, it steals your energy and vigor over months and sometimes years. DEFINITION: Just for a sake of clarity, the name of this illness has brought a lot of controversy, and currently they are trying to change it to neuroendocrineimmune dysfunction syndrome, or NDS, which better reflects the symptoms of this illness, is not just fatigue… Chronic Fatigue Syndrome is an Illness characterized by a permanent fatigue (that it does not improve with the rest), for at least six consecutive months, accompanied of other symptoms as difficulty of concentration, lost of memory, non-refreshing sleep, muscular pains, pains you will articulate (without inflammation), migraines, general discomfort post exercise that extends more than 24 hours and alterations of the sleep. This Chronic Fatigue Syndrome has also been called Immune Malfunction, epidemic Neuromiastenia and Myalgic Encephalomyelitis. CAUSES: There is not known yet the final cause of it, but it is believed that a viral infection is involved in it. Among the viruses responsible for CFS are: Epstein-Barr, HIV, HHV-6, Cytomegalovirus, retrovirus or enterovirus. The World Health Organization has listed the discrete disease, CFS under neurological disorders specifically excluding it from psychiatric disorders. Doctors treating patients medically diagnosed with CFS describe them as more functionally ill than cancer patients undergoing chemotherapy, patients with HIV, Type 2 diabetes and another neurological disorder MS. In one study, Ablashi et al. (15) found that 25% of the serum 300 CFS patients, tested for HHV-6 IgG and EBV-VCA IgG antibody, showed elevated antibodies to both HHV-6 and EBV. Most of us have already been infected with the virus in our first year of life. In most individuals the virus is latent. When HHV-6 is reactivated, or during reinfection, it may contribute to CFS. Evidence of the involvement of HHV-6 in CFS, compared to that of other human herpes viruses (EBV, CMV, HSV-1 and 2, VZV, HHV-7), is much stronger. The evidence is based on: 1. Elevated IgG antibody; 2. Detection of anti-IgM antibody in equal to or less than 50% of patients, which is a good indication of virus reactivation; 3. Detection of HHV-6 antigen expressing cells in the peripheral blood mononuclear cells of CFS patients by culture techniques; 4. Detection of HHV-6 DNA in lymphocytes of CFS patients by PCR and Southern blot hybridization (22-23,33,35-36). DIAGNOSTIC AND BIOLOGICAL MARKERS: A)Diagnostic Valuable Test Although not generally accepted as a diagnostic test, they havebeen claimed by researchers to be useful markers for the disease and tend to be present in most of the patients. Nevertheless the value of these is more for diagnosis than for treatment of the condition.In order of importance: Mitochondrial Profile, H2S in urine, RNASe-L, PKR and Elastase levels, Nitric Oxide in serum and oxidation levels, SPECT andxenon SPECT scans of the brain, MRI scans of the brain, PET scans of the brain, Neuropsychological testing, EEG brain maps and QEEG brain maps, Erythrocyte sedimentation rate (ESR), Insulin levels and glucose tolerance tests, 24-Hour Holter monitor, Tilt table examination, Exercise testing and chemical stress tests, Neurological examination and the Romberg or tandem Romberg test. B)Aditional abnormalities test found in CFS patients should be checked at least once, and based on the criteria of the physician that is treating you, it might be necessary to repeat them periodically to evaluate the evolution of the protocol followed in your case. -Tests of the immune system: The Th1-Th2 relationship of the immune system, Low NK activity (as opposed to levels), T-Activated Linfocites Count, % Linfocites, Cellular Inversion at CHMI and/or CHMII level, Elevations of circulating cytokines, Immunoglobulin deficiencies -Serology Test: IgG for viruses such as Epstein-Barr, CMV, HHV6. Additionally we need to get tested for all possible infections that could have caused a reaction in our hormonal stress, and therefore in the serology we should include: mononucleosis, Hepatitis B & C, LES markers, Toxoplasma, antibodies of candida albicans, Babesia, Erchilia, Bartonella, Borrelia etc… -Levels of amino acids in blood and urine 24h or spot. -Liver function -Candida levels, in order to detect subclinical fungi infections like candida albicans, there are special urine test that measure the metabolites that will help us to rule it out it also can be observed the metabolites through an Organic Acids Test. According to the results, patients should seek be treated for each one of the abnormalities which show up. There are allopathic treatments (can be problematic for some, as CFS-MEers tend to have also Chemical Sensitivities) or homeopathic treatments (in Germany, they are very commonly used). Diet is also important regarding dealing with chemical sensitivities, amino acid levels, candida levels. C) Advance testing on CFS: Besides theses regular, although not standard test mentioned above, there are additional test that can be run, and will deliver relevant input for CFS patients. There is a protocol to regulate these different abnormalities, which might be causing part of the symptoms in CFS, as a few of the latest research published postulates. We will discuss below some of them in here: -Mitochondrial Profile This is in the latest research the main responsible for CFS. There is a test run in UK by Dr. Myhill. This test measures the enzyme SODase (Superoxide Dismutasa) This enzyme is necessary in the detox process of free radicals of the mitochondria, as well as the CoQ10 levels, Niacinamide and Intracellular Magnesium. And most of all the efficiency of the mitochondria in converting ADP into ATP. It also measures the free ADN which is a nice marker to observe the cellular damage and apoptosis or PKRwhich is the programmed cellular death due to oxidative stress. -Adrenal Hormones in Saliva: This test is useful to treat the adrenal failure, because there is a treatment for it. The test is run during a whole day (8:00, 12:00, 16:00, 20:00) Cortisol and DHEA levels are tested. Also is necessary to test for a potential subclinical Thyroids problem (TSH, T3 and T4). Preferably in urine 24h, because subclinical thyroids is not always detectable in serum. Additionally a hair mineral test can be done to observe the unbalance existing in terms of minerals caused by suprarenal malfunction and correct it accordingly. -HPU Test: This test measures a metabolic disorder, often occuring as a biochemical-enzymatic familiarly during the chemical reaction of formation of the red blood pigment. (Hemosynthesis). It can be said that Kryptopyrrolurea is not a symptom, but rather the primal cause for different symptoms and disease states, among others hipoglucemia. In the German-speaking countries, is abbreviated as KPU. In the Netherlands HPU. In England the abbreviation is HPL. -Hypercoagulation Testing: As a part of Hemex's research, they have developed a test to determine if a patient has this hypercoagulation disorder. The Immune System Activation of Coagulation (ISAC) tests five substances; abnormal results on any two of the five is considered to be a positive indicator of hypercoagulation. Their results thus far have found 79-92 percent of the CFS and/or FM patients they tested have hypercoagulation. As with many of the more detailed blood tests developed in the past decade, the defects causing hypercoagulation are rarely or not at all detectable by the standard laboratory tests performed at general labs, such as Unilab, Quest Diagnostics, etc. The standard coagulation workup done by these labs assess only the risk of actual clotting, whereas the ISAC panel is 10-20 times more sensitive. -Metilation Panel (methionine cycle): This blood test is meant to observe the potential blockage of the methylation cycle, and therefore the potential detox treatment and follow up through urine. If after this analysis, you observe a blocked Methylation Cycle, then is wise to do a metal in urine test to have a starting point for the detox treatment. This test will be useful to follow up the metal excretion in the detox protocol or / and adapt the mineral doses intake. The role of the methylation cycle in the sulfur metabolism is to supply sulfur-containing metabolites to form a variety of important substances, including cysteine, glutathione, taurine and sulfate, via its connection with the transsulfuration pathway. In autism the methylation cycle was found to be blocked at methionine synthase, which is the step involving methylation of homocysteine to form methionine, resulting in lower plasma levels of cysteine and glutathione and a lowered ratio of reduced to oxidized glutathione. This lowered ratio reflects a state of oxidative stress. It is known from studies of twins that genetics plays an important predisposing role in autism.The fact that the rate of incidence of autism has increased dramatically in recent years is evidence that there is also an important environmental component in the development of cases of autism, since the population's genetic inheritance is relatively constant over much longer periods. Evidence suggests that this same dysfunction is also present in chronic fatigue syndrome: Low methionine levels in serum and urine, below-normal levels of carnitine, coenzyme Q10 and melatonin. All these substances require methylation for their biosynthesis. RNase-L remains activated in CFS because of the suppression of the cell-mediated immune response and the consequent failure to defeat the viral infection There is abundant and compelling evidence that the glutathione depletion methylation cycle block mechanism is an important part of the pathogenesis for at least a substantial subset of chronic fatigue syndrome patients. -Glutathione and Selenium Test: The best complement to Methylation Panel, would be to check Reduced Glutathione RBC GSH, Oxidated Glutathione (RBC GSSG) and Total Glutathione (RBC). The important one is RBC GSH, and also the ratio of this one versus RBC GSSG. This is relevant given that the low levels of glutathione due to the blocked methylation cycle, is the main responsible for the symptoms of CFS. In the initial states of oxidative stress in this illness Total Glutathione could be miss leading and be normal or even high, that is why we test for the other two as well. Besides, even if Glutathione comes normal, if Selenium level is low, the enzymes could not work properly. Depletion of reduced glutathione likewise causes a shift to Th2. Depletion of reduced glutathione is the trigger for the reactivation of latent viral and intracellular bacteria in CFS. In general, intracellular glutathione depletion is associated with the activation of several types of viruses. It is likely that glutathione depletion is responsible for reactivation of Epstein-Barr virus, cytomegalovirus and HHV-6 in CFS. Populations more deficient in selenium would be expected to be more vulnerable to Coxsackie B3 infection. Read more: http://www.bukisa.co...e#ixzz0woSFZ3GS

You may have another appointment, but that appointment will be to determine if you should be paid at the 100% TDIU rate. I think you should be fine. VA just awarded your claim for PTSD, they will not try to mess with it this soon.

Berta, I think you and Fire Courage are talking about two different things. I think Fire Courage is talking about everything the VAMC hospital has diagnosed him with. He can go to the VAMC hospital and ask the ROI office for a copy of a diagnosis sheet, he will have to sign something and they will print it out. It normally comes on one sheet of paper but sometimes they (ROI) office will print out a bunch of sheets with only one or two diagnosis but he would have to read all of them to know what is going on. Berta, you are talking about the complete rating decision that includes the legend which is the regional office sheets thats list all the service connected and non-service connected disabilities/conditions. It also shows the rating percentages and their effective dates and it can be blue. Hope this Helps

Can you be a little more clearer? Keep in mind that no one knows you here but we would need more information and it could help other veterans. What claim did you file and what conditions do you have on appeal.

The veteran filed a NOD and depending on the outcome the veteran can get an award of TDIU for 2006.

When was the veteran awarded 70% for PTSD? Did the VA consider TDIU at the same time the veteran was awarded 70% for PTSD? It really does make a difference.

You will have to go to the VA and they have service officers there or you can try to get one at your local county. I think that the local county service officer will not go with you to your hearing but they will help you put your claim together.

The DRO process is "supposed" to be faster but beware, they like to rubber stamp your claim. In some cases veterans do win but you will have to have all your information together. Do you have a good service officer to help you?

John, I totally agree. I do not have a lawyer but I am waiting for VA to decide my CUE claims. I filed them in 2006 and they have been back and forth from the RO to BVA to the RO back to BVA and now back to the RO again. I am hoping that I get a decent rating and not just a rubber stamp. I am very glad that BVA did not agree with the original VA decision and remanded my claims. It makes me feel that my claims are legitimate since all the evidence was in my records and they denied/low balled my claims knowing the condition and the things I have been going through. It just rubs me the wrong way and I can't even imagine if they had made the right decision years ago I could be in a better situation. Please keep me posted, I am really interested in what VA will say about your claim. I think that we are in the same boat or at least it seems like the same boat.

Don't worry just yet, keep in mind if you don't like the decision, your claim can still go back to BVA.

Agent Orange Claims Update August 20, 2010 posted by Chuck Palazzo · From the DVA newsletter, Agent Orange Review: Three new presumptives will indeed be part of the list later in 2010. As always, I urge you to get your claims submitted. This newsletter, although not law, does come from the DVA and is a pretty good indicator of what will follow. The Department of Veterans Affairs (VA) will add two new conditions to the list of“presumptive illnesses” related to Agent Orange exposure. These are Parkinson’sdisease and ischemic heart disease. In addition, VA will expand the presumption for chronic lymphocytic leukemia to include all chronic B-cell leukemias, such as hairy cell leukemia. These conditions will now be presumed to be service-connected to herbicide exposure in Vietnam. Vietnam Veterans with these illnesses will be able to claim VA disability benefits and health care services without having to prove that their conditions are connected to Agent Orange exposure. The new policy,expected to take effect in late 2010, will apply to Veterans who served in Vietnam anytime during the period beginning January 9, 1962, and ending on May 7, 1975. It will not apply to Veterans who only served on “Blue Water”Navy ships in the region. “We must do better reviews of illnesses that may be connected to service, and we will,” said Secretary of Veterans Affairs Eric K. Shinseki. “Veterans who endure health problems deserve timely decisions based on solid evidence.”

Important Research Studies That Point to Hope for Chronic Fatigue August 20, 2010 posted by Denise Nichols Fourteen studies that give hope to Gulf War Veterans with Chronic Fatigue Fourteen studies over a year that are helping to lead the way to answers for Chronic Fatigue and Gulf War Veterans are highlighted below. Significant work is occurring on finding biomarkers, genetic markers, potentials for treatment, and future direction in this field of research. The significant findings are underlined in the abstracts, to help guide the non medical person to the take away message. Dr Klimas and Dr Baraniuk are in the lead here in the United States besides studies at Wayne State, Seattle, and Chicago but this is a significant list of research centers that is international with UK, Australia, Canada, India, and Belgium represented. 1. Allergy Asthma Proc. 2010 May-Jun;31(3):169-78. Relationships among rhinitis, fibromyalgia, and chronic fatigue. Baraniuk JN, Zheng Y. Division of Rheumatology, Immunology and Allergy, Georgetown University, PHC Building, 3800 Reservoir Road, NW, Washington, DC 20007-2197, USA. Abstract New information about the pathophysiology of idiopathic nonallergic rhinopathy indicates a high prevalence in chronic fatigue syndrome (CFS). This article shows the relevance of CFS and allied disorders to allergy practice. CFS has significant overlap with systemic hyperalgesia (fibromyalgia), autonomic dysfunction (irritable bowel syndrome and migraine headaches), sensory hypersensitivity (dyspnea; congestion; rhinorrhea; and appreciation of visceral nociception in the esophagus, gastrointestinal tract, bladder, and other organs), and central nervous system maladaptations (central sensitization) recorded by functional magnetic resonance imaging (fMRI). Neurological dysfunction may account for the overlap of CFS with idiopathic nonallergic rhinopathy. Scientific advances are in fMRI, nociceptive sensor expression, and, potentially, infection with xenotropic murine leukemia-related virus provide additional insights to novel pathophysiological mechanisms of the “functional” complaints of these patients that are mistakenly interpreted as allergic syndromes. As allergists, we must accept the clinical challenges posed by these complex patients and provide proper diagnoses, assurance, and optimum care even though current treatment algorithms are lacking. 1 selected item: 20629967FormatSummarySummary (text)AbstractAbstract (text)MEDLINEXMLPMID 2. Pain Pract. 2010 Jan-Feb;10(1):54-9. Treatment of the narcoleptiform sleep disorder in chronic fatigue syndrome and fibromyalgia with sodium oxybate. Spitzer AR, Broadman M. Neurology Department, Wayne State University School of Medicine, Detroit, Michigan, USA. Abstract This study investigates the response of the underlying sleep disorder associated with Chronic Fatigue Syndrome (CFS) and fibromyalgia (FM) to treatment. We retrospectively reviewed 118 cases clinically consistent with CFS or FM, treated in a neurology practice. Abnormal findings on sleep studies and associated human leukocyte antigen markers, and a clinical pattern suggestive of narcolepsy, are present in a high proportion of patients. When considered appropriate based on the clinical picture and test results, treatment with sodium oxybate was offered to these patients. Sixty percent of patients treated with oxybate experienced significant relief of pain, while 75% experienced significant relief of fatigue. We postulate that the response to oxybate in CFS and FM suggests a disturbance of sleep similar to narcolepsy. These findings support this novel approach to intervention and further research. The inability to distinguish CFS and FM by testing and response to treatment suggests that they may represent variations of the same disorder or may be closely related disorders. PMID: 20629967 [PubMed - in process] 3. Prog Neuropsychopharmacol Biol Psychiatry. 2010 Jul 4. [Epub ahead of print] An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways. Maes M. Abstract There is a significant ‘comorbidity’ between depression and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Depressive symptoms frequently occur during the course of ME/CFS. Fatigue and somatic symptoms (F&S), like pain, muscle tension, and a flu-like malaise, are key components of depression. At the same time, depression and ME/CFS show major clinical differences, which allow to discriminate them with a 100% accuracy. This paper aims to review the shared pathways that underpin both disorders and the pathways that discriminate them. Numerous studies have shown that depression and ME/CFS are characterized by shared aberrations in inflammatory, oxidative and nitrosative (IO&NS) pathways, like systemic inflammation and its long-term sequels, including O&NS-induced damage to fatty acids, proteins and DNA; dysfunctional mitochondria; lowered antioxidant levels, like zinc and coenzyme Q10; autoimmune responses to neoepitopes formed by O&NS; lowered omega-3 polyunsaturated fatty acid levels; and increased translocation of gram-negative bacteria. Some IO&NS-related pathways, like the induction of indoleamine 2-3-dioxygenase, neurodegeneration and decreased neurogenesis, are more specific to depression, whereas other pathways, like the 2′-5′ oligoadenylate synthetase/RNase L pathway, are specific to ME/CFS. Most current animal models of depression, e.g. those induced by cytokines, are not reminiscent of human depression but reflect a mixture of depressive and F&S symptoms. The latter symptoms, sometimes called sickness behavior, differ from depression and ME/CFS because the former is a (sub)acute response to infection-induced pro-inflammatory cytokines that aims to enhance recovery, whereas the latter are characterized by long-term sequels in multiple IO&NS pathways. Depression and ME/CFS are not ‘comorbid’ disorders, but should be regarded as ‘co-associated disorders’ that are clinical manifestations of shared pathways. PMID: 20609377 [PubMed - as supplied by publisher] 4. Inflammopharmacology. 2010 Jul 3. [Epub ahead of print] Potential role of pioglitazone, caffeic acid and their combination against fatigue syndrome-induced behavioural, biochemical and mitochondrial alterations in mice. Kumar A, Vashist A, Kumar P. Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, 160014, India Abstract Chronic fatigue is an illness characterised by persistent and relapsing fatigue, often accompanied by numerous neuropsychiatric problems, such as anxiety and depression. The aetiology of chronic fatigue remains unclear so far. However, recent studies suggested the involvement of oxidative stress in this chronic debilitating disease. Alternatively, antioxidants have also been reported to have beneficial effect against chronic fatigue-like conditions. Therefore, present study has been designed to explore the potential role of pioglitazone, caffeic acid and their combination against chronic fatigue-like condition in mice. In the experimental protocol, the mice were put on the running wheel apparatus for 6 min test session daily for 21 days which produced fatigue-like condition. The locomotor activity and anxiety levels were measured on 0, 8th, 15th and 22nd days. The brains were isolated on 22nd day immediately after the behavioural assessments, oxidative damage and mitochondrial enzyme complexes were then estimated subsequently. Three weeks pioglitazone (5 and 10 mg/kg) and caffeic acid (5 and 10 mg/kg) pretreatment significantly attenuated the chronic fatigue-like condition (restored running wheel activity, locomotor activity and reduced anxiety-like behaviour) as compared to that in control (chronic fatigue) animals. Further, pioglitazone (5 and 10 mg/kg) and caffeic acid (5 and 10 mg/kg) drug treatments for 3 weeks significantly attenuated oxidative damage (decreased lipid peroxidation, nitrite concentration, restored reduction in glutathione and catalase levels), altered mitochondrial enzymes complex (I, II and IV) activities and mitochondrial redox activity (MTT assay) when compared with control. Further, combination of lower dose of pioglitazone (5 mg/kg) and caffeic acid (5 mg/kg) showed significant synergism in their protective effect which was significant as compared to their effect per se. The present study highlights the potential role of pioglitazone, caffeic acid and their combination in the pathophysiology of chronic fatigue-like condition in mice. PMID: 20602174 [PubMed - as supplied by publisher] 5. J Neuroimmunol. 2010 May 25. [Epub ahead of print] Possible role of oxidative stress and immunological activation in mouse model of chronic fatigue syndrome and its attenuation by olive extract. Gupta A, Vij G, Chopra K. Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Center of Advanced Study, Panjab University, Chandigarh 160014, India. Abstract Various putative theories involved in the development of chronic fatigue syndrome revolve around the role of stress, infection and oxidative stress. Scientific evidence highlighting the protective role of nutritional supplements in chronic fatigue syndrome is lacking. Based on these assumptions, the present study was designed to evaluate the effect of olive extract in a mouse model of immunologically-induced fatigue, wherein purified lipopolysaccharide (LPS) and Brucella abortus (BA) antigen were used as immunogens. The assessment of chronic fatigue syndrome was based on immobility period during chronic water-immersion stress test for 10min daily. The stress-induced hyperalgesia was measured by tail withdrawal latency. Mice challenged with LPS or BA for 19days showed significant increase in the immobility time, hyperalgesia and oxidative stress on the 19th day. Serum tumor necrosis factor-alpha (TNF-alpha) levels were also markedly increased with LPS or BA challenge. Concurrent treatment with olive extract resulted in a significant decrease in the immobility time as well as hyperalgesia. There was significant attenuation of oxidative stress as well as serum TNF-alpha levels. The results of the present study strongly indicate the role of oxidative stress and immunological activation in the pathophysiology of chronic fatigue syndrome and highlight the valuable role of olive extract in combating chronic fatigue syndrome. PMID: 20537729 [PubMed - as supplied by publisher] 6. PLoS One. 2010 May 25;5(5):e10817. Biomarkers in chronic fatigue syndrome: evaluation of natural killer cell function and dipeptidyl peptidase IV/CD26. Fletcher MA, Zeng XR, Maher K, Levis S, Hurwitz B, Antoni M, Broderick G, Klimas NG. Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA. Abstract BACKGROUND: Chronic Fatigue Syndrome (CFS) studies from our laboratory and others described decreased natural killer cell cytotoxicity (NKCC) and elevated proportion of lymphocytes expressing the activation marker, dipeptidyl peptidase IV (DPPIV) also known as CD26. However, neither these assays nor other laboratory tests are widely accepted for the diagnosis or prognosis of CFS. This study sought to determine if NKCC or DPPIV/CD26 have diagnostic accuracy for CFS. METHODS/RESULTS: Subjects included female and male CFS cases and healthy controls. NK cell function was measured with a bioassay, using K562 cells and (51)Cr release. Lymphocyte associated DPPIV/CD26 was assayed by qualitative and quantitative flow cytometry. Serum DPPIV/CD26 was measured by ELISA. Analysis by receiver operating characteristic (ROC) curve assessed biomarker potential. Cytotoxic function of NK cells for 176 CFS subjects was significantly lower than in the 230 controls. According to ROC analysis, NKCC was a good predictor of CFS status. There was no significant difference in NK cell counts between cases and controls. Percent CD2+ lymphocytes (T cells and NK cells) positive for DPPIV/C26 was elevated in CFS cases, but there was a decrease in the number of molecules (rMol) of DPPIV/C26 expressed on T cells and NK cells and a decrease in the soluble form of the enzyme in serum. Analyses by ROC curves indicated that all three measurements of DPPIV/CD26 demonstrated potential as biomarkers for CFS. None of the DPPIV/C26 assays were significantly correlated with NKCC. CONCLUSIONS: By ROC analysis, NKCC and three methods of measuring DPPIV/C26 examined in this study had potential as biomarkers for CFS. Of these, NKCC, %CD2+CD26+ lymphocytes and rMol CD26/CD2+ lymphocyte, required flow cytometry, fresh blood and access to a high complexity laboratory. Soluble DPPIV/C26 in serum is done with a standard ELISA assay, or with other soluble factors in a multiplex type of ELISA. Dipeptidyl peptidase IV on lymphocytes or in serum was not predictive of NKCC suggesting that these should be considered as non-redundant biomarkers. Abnormalities in DPPIV/CD26 and in NK cell function have particular relevance to the possible role of infection in the initiation and/or the persistence of CFS. PMID: 20520837 [PubMed - in process]PMCID: PMC2876037Free PMC Article 7. Brain Behav Immun. 2010 May 4. [Epub ahead of print] A formal analysis of cytokine networks in Chronic Fatigue Syndrome. Broderick G, Fuite J, Kreitz A, Vernon SD, Klimas N, Fletcher MA. Department of Medicine, University of Alberta, Edmonton, Alberta, Canada. Abstract Chronic Fatigue Syndrome (CFS) is a complex illness affecting 4 million Americans for which no characteristic lesion has been identified. Instead of searching for a deficiency in any single marker, we propose that CFS is associated with a profound imbalance in the regulation of immune function forcing a departure from standard pre-programmed responses. To identify these imbalances we apply network analysis to the co-expression of 16 cytokines in CFS subjects and healthy controls. Concentrations of IL-1a, 1b, 2, 4, 5, 6, 8, 10, 12, 13, 15, 17 and 23, IFN-gamma, lymphotoxin-alpha (LT-alpha) and TNF-alpha were measured in the plasma of 40 female CFS and 59 case-matched controls. Cytokine co-expression networks were constructed from the pair-wise mutual information (MI) patterns found within each subject group. These networks differed in topology significantly more than expected by chance with the CFS network being more hub-like in design. Analysis of local modularity isolated statistically distinct cytokine communities recognizable as pre-programmed immune functional components. These showed highly attenuated Th1 and Th17 immune responses in CFS. High Th2 marker expression but weak interaction patterns pointed to an established Th2 inflammatory milieu. Similarly, altered associations in CFS provided indirect evidence of diminished NK cell responsiveness to IL-12 and LT-alpha stimulus. These observations are consistent with several processes active in latent viral infection and would not have been uncovered by assessing marker expression alone. Furthermore this analysis identifies key sub-networks such as IL-2:IFN-gamma:TNF-alpha that might be targeted in restoring normal immune function. PMID: 20447453 [PubMed - as supplied by publisher] 8. J Intern Med. 2010 Apr;267(4):394-401. Abnormalities in pH handling by peripheral muscle and potential regulation by the autonomic nervous system in chronic fatigue syndrome. Jones DE, Hollingsworth KG, Taylor R, Blamire AM, Newton JL. Institute of Cellular Medicine, Newcastle University, Newcastle-upon-Tyne, UK. Abstract OBJECTIVES: To examine muscle acid handling following exercise in chronic fatigue syndrome (CFS/ME) and the relationship with autonomic dysfunction. DESIGN: Observational study. SETTING: Regional fatigue service. SUBJECTS & INTERVENTIONS: Chronic fatigue syndrome (n = 16) and age and sex matched normal controls (n = underwent phosphorus magnetic resonance spectroscopy (MRS) to evaluate pH handling during exercise. Subjects performed plantar flexion at fixed 35% load maximum voluntary contraction. Heart rate variability was performed during 10 min supine rest using digital photophlethysmography as a measure of autonomic function. RESULTS: Compared to normal controls, the CFS/ME group had significant suppression of proton efflux both immediately postexercise (CFS: 1.1 +/- 0.5 mmol L(-1) min(-1) vs. normal: 3.6 +/- 1.5 mmol L(-1) min(-1), P < 0.001) and maximally (CFS: 2.7 +/- 3.4 mmol L(-1) min(-1) vs. control: 3.8 +/- 1.6 mmol L(-1) min(-1), P < 0.05). Furthermore, the time taken to reach maximum proton efflux was significantly prolonged in patients (CFS: 25.6 +/- 36.1 s vs. normal: 3.8 +/- 5.2 s, P < 0.05). In controls the rate of maximum proton efflux showed a strong inverse correlation with nadir muscle pH following exercise (r(2) = 0.6; P < 0.01). In CFS patients, in contrast, this significant normal relationship was lost (r(2) = 0.003; P = ns). In normal individuals, the maximum proton efflux following exercise were closely correlated with total heart rate variability (r(2) = 0.7; P = 0.007) this relationship was lost in CFS/ME patients (r(2) < 0.001; P = ns). CONCLUSION: Patients with CFS/ME have abnormalities in recovery of intramuscular pH following standardised exercise degree of which is related to autonomic dysfunction. This study identifies a novel biological abnormality in patients with CFS/ME which is potentially open to modification. PMID: 20433583 [PubMed - indexed for MEDLINE] 9. J Altern Complement Med. 2010 Mar;16(3):235-49. Alternative medical interventions used in the treatment and management of myalgic encephalomyelitis/chronic fatigue syndrome and fibromyalgia. Porter NS, Jason LA, Boulton A, Bothne N, Coleman B. Center for Community Research, DePaul University, Chicago, IL 60614, USA. Abstract BACKGROUND: There have been several systematic reviews attempting to evaluate the efficacy of possible treatments for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM). However, information regarding the efficacy of complementary and alternative medicine (CAM) has not been comprehensively or systematically covered in these reviews, despite its frequent use in the patient community. PURPOSE: The purpose of this study was to systematically review and evaluate the current literature related to alternative and complementary treatments for ME/CFS and FM. It should be stressed that the treatments evaluated in this review do not reflect the clinical approach used by most practitioners to treat these illnesses, which include a mix of natural and unconventionally used medications and natural hormones tailored to each individual case. However, nearly all clinical research has focused on the utility of single CAM interventions, and thus is the primary focus of this review. METHODS: Several databases (e.g., PubMed, MEDLINE,(®) PsychInfo) were systematically searched for randomized and nonrandomized controlled trials of alternative treatments and nonpharmacological supplements. Included studies were checked for references and several experts were contacted for referred articles. Two leading subspecialty journals were also searched by hand. Data were then extracted from included studies and quality assessments were conducted using the Jadad scale. RESULTS: Upon completion of the literature search and the exclusion of studies not meeting criterion, a total of 70 controlled clinical trials were included in the review. Sixty (60) of the 70 studies found at least one positive effect of the intervention (86%), and 52 studies also found improvement in an illness-specific symptom (74%). The methodological quality of reporting was generally poor. CONCLUSIONS: Several types of alternative medicine have some potential for future clinical research. However, due to methodological inconsistencies across studies and the small body of evidence, no firm conclusions can be made at this time. Regarding alternative treatments, acupuncture and several types of meditative practice show the most promise for future scientific investigation. Likewise, magnesium, l-carnitine, and S-adenosylmethionine are nonpharmacological supplements with the most potential for further research. Individualized treatment plans that involve several pharmacological agents and natural remedies appear promising as well. PMID: 20192908 [PubMed - indexed for MEDLINE] 10. J Affect Disord. 2010 Sep;125(1-3):287-294. Epub 2010 Jan 18. Increased plasma peroxides and serum oxidized low density lipoprotein antibodies in major depression: Markers that further explain the higher incidence of neurodegeneration and coronary artery disease. Maes M, Mihaylova I, Kubera M, Uytterhoeven M, Vrydags N, Bosmans E. Maes Clinics, Belgium. Abstract BACKGROUND: Major depression is characterized by a decreased antioxidant status, an induction of the inflammatory and oxidative and nitrosative (IO&NS) pathways and inflammatory-neurodegenerative (I&ND) pathways. This study examines two markers of oxidative stress in depression, i.e. plasma peroxides and serum oxidized LDL (oxLDL) antibodies. METHODS: Blood was sampled in 54 patients with major depression (mean+/-SD age=43.5+/-11.6years) and 37 normal volunteers (43.6+/-11.1years). The severity of illness was measured by means of the Hamilton Depression Rating Scale. The Fibromyalgia and Chronic Fatigue Syndrome Rating Scale was used to measure severity of “psychosomatic” symptoms in depression. RESULTS: We found significantly higher plasma peroxides (p=0.002) and serum oxLDL antibodies (p=0.0002) in depressed patients as compared to normal controls. There was no significant correlation between both markers and both independently from each other predicted major depression. There were significant correlations between the oxLDL antibodies and the scores on two items of the FF scale, i.e. gastro-intestinal symptoms and headache. DISCUSSION: The results show that major depression is accompanied by increased oxidative stress and lipid peroxidation. These results further extend the IO&NS pathophysiology of major depression. Since increased peroxides and oxLDL antibodies are predictors of coronary artery disease (CAD) and neurodegeneration, our findings suggest that IO&NS pathways are involved in the increased incidence of both CAD and neurodegeneration in depression. PMID: 20083310 [PubMed - as supplied by publisher] 11. J Transl Med. 2010 Jan 11;8:1. Immune and hemorheological changes in chronic fatigue syndrome. Brenu EW, Staines DR, Baskurt OK, Ashton KJ, Ramos SB, Christy RM, Marshall-Gradisnik SM. Faculty of Health Science and Medicine, Population Health and Neuroimmunology Unit, Bond University, Robina, Queensland, Australia. Abstract BACKGROUND: Chronic Fatigue Syndrome (CFS) is a multifactorial disorder that affects various physiological systems including immune and neurological systems. The immune system has been substantially examined in CFS with equivocal results, however, little is known about the role of neutrophils and natural killer (NK) phenotypes in the pathomechanism of this disorder. Additionally the role of erythrocyte rheological characteristics in CFS has not been fully expounded. The objective of this present study was to determine deficiencies in lymphocyte function and erythrocyte rheology in CFS patients. METHODS: Flow cytometric measurements were performed for neutrophil function, lymphocyte numbers, NK phenotypes (CD56(dim)CD16(+) and CD56(bright)CD16(-)) and NK cytotoxic activity. Erythrocyte aggregation, deformability and fibrinogen levels were also assessed. RESULTS: CFS patients (n = 10) had significant decreases in neutrophil respiratory burst, NK cytotoxic activity and CD56(bright)CD16(-) NK phenotypes in comparison to healthy controls (n = 10). However, hemorheological characteristic, aggregation, deformability, fibrinogen, lymphocyte numbers and CD56(dim)CD16(+) NK cells were similar between the two groups. CONCLUSION: These results indicate immune dysfunction as potential contributors to the mechanism of CFS, as indicated by decreases in neutrophil respiratory burst, NK cell activity and NK phenotypes. Thus, immune cell function and phenotypes may be important diagnostic markers for CFS. The absence of rheological changes may indicate no abnormalities in erythrocytes of CFS patients. PMID: 20064266 [PubMed - indexed for MEDLINE]PMCID: PMC2829521Free PMC Article 12. Am J Med. 2009 Dec;122(12 Suppl):S44-55. Further strategies for treating fibromyalgia: the role of serotonin and norepinephrine reuptake inhibitors. Mease PJ. Seattle Rheumatology Associates, Swedish Medical Center, Seattle, Washington, USA. Abstract Fibromyalgia and associated conditions such as irritable bowel syndrome and temporomandibular disorder involve dysfunctions in central sensitization and pain modulation. Central nervous system dysfunction may also contribute to other symptoms characteristic of fibromyalgia, such as fatigue and sleep disturbance. Two key neurotransmitters in the pain modulation pathway are serotonin and norepinephrine. Preclinical studies using animal models of chronic pain have shown that pharmacologic agents that combine serotonergic and noradrenergic reuptake inhibition, thus augmenting the function of these neurotransmitters, have stronger analgesic effects than agents that inhibit reuptake of either neurotransmitter alone. Although tricyclic antidepressants (TCAs) inhibit reuptake of both serotonin and norepinephrine and have shown efficacy for the treatment of fibromyalgia, long-term use of these drugs is limited owing to poor tolerability. Unlike TCAs, the newer dual reuptake inhibitors of serotonin and norepinephrine, such as the drugs approved by the US Food and Drug Administration (FDA) for fibromyalgia, milnacipran and duloxetine, do not possess significant affinity for other neurotransmitter systems, resulting in diminished side effects and enhanced tolerability. Both duloxetine and milnacipran have shown efficacy in clinical trials by improving pain and other symptoms associated with fibromyalgia. Both compounds inhibit the serotonin and norepinephrine transporters; however, there is a difference in their affinities and selectivity for these transporters. Although duloxetine has affinity for both receptors, it is somewhat more selective for the serotonin transporter. In contrast, milnacipran is somewhat more selective for norepinephrine than serotonin reuptake inhibition. Pharmacologic agents that specifically target serotonin and norepinephrine reuptake may prove to be valuable tools in the treatment of fibromyalgia. PMID: 19962496 [PubMed - indexed for MEDLINE] 13. Neuro Endocrinol Lett. 2009;30(4):470-6. Coenzyme Q10 deficiency in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardiovascular disorder. Maes M, Mihaylova I, Kubera M, Uytterhoeven M, Vrydags N, Bosmans E. Maes Clinics, Antwerp, Belgium. Abstract INTRODUCTION: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a medical illness characterized by disorders in inflammatory and oxidative and nitrosative (IO&NS) pathways. METHODS: This paper examines the role of Coenzyme Q10 (CoQ10), a mitochondrial nutrient which acts as an essential cofactor for the production of ATP in mitochondria and which displays significant antioxidant activities. Plasma CoQ10 has been assayed in 58 patients with ME/CFS and in 22 normal controls; the relationships between CoQ10 and the severity of ME/CFS as measured by means of the FibroFatigue (FF) scale were measured. RESULTS: Plasma CoQ10 was significantly (p=0.00001) lower in ME/CFS patients than in normal controls. Up to 44.8% of patients with ME/CFS had values beneath the lowest plasma CoQ10 value detected in the normal controls, i.e. 490 microg/L. In ME/CFS, there were significant and inverse relationships between CoQ10 and the total score on the FF scale, fatigue and autonomic symptoms. Patients with very low CoQ10 (<390 microg/L) suffered significantly more from concentration and memory disturbances. DISCUSSION: The results show that lowered levels of CoQ10 play a role in the pathophysiology of ME/CFS and that symptoms, such as fatigue, and autonomic and neurocognitive symptoms may be caused by CoQ10 depletion. Our results suggest that patients with ME/CFS would benefit from CoQ10 supplementation in order to normalize the low CoQ10 syndrome and the IO&NS disorders. The findings that lower CoQ10 is an independent predictor of chronic heart failure (CHF) and mortality due to CHF may explain previous reports that the mean age of ME/CFS patients dying from CHF is 25 years younger than the age of those dying from CHF in the general population. Since statins significantly decrease plasma CoQ10, ME/CFS should be regarded as a relative contraindication for treatment with statins without CoQ10 supplementation. PMID: 20010505 [PubMed - indexed for MEDLINE] 14. J Clin Pathol. 2010 Feb;63(2):156-64. Epub 2009 Dec 2. Microbial infections in eight genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis. Zhang L, Gough J, Christmas D, Mattey DL, Richards SC, Main J, Enlander D, Honeybourne D, Ayres JG, Nutt DJ, Kerr JR. Department of Cellular & Molecular Medicine, St George’s University of London, London, UK. Abstract BACKGROUND: The authors have previously reported genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) based on expression of 88 human genes. AIM: To attempt to reproduce these findings, determine the specificity of this signature to CFS/ME, and test for associations between CFS/ME subtype and infection. METHODS: Expression levels of 88 human genes were determined in blood of 62 new patients with idiopathic CFS/ME (according to Fukuda criteria), six patients with Q-fever-associated CFS/ME from the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous depression (according to DSM-IV criteria) and 29 normal blood donors. RESULTS: In patients with CFS/ME, differential expression was confirmed for all 88 genes. Q-CFS/ME had similar patterns of gene expression to idiopathic CFS/ME. Gene expression in patients with endogenous depression was similar to that in the normal controls, except for upregulation of five genes (APP, CREBBP, GNAS, PDCD2 and PDCD6). Clustering of combined gene data in CFS/ME patients for this and the authors’ previous study (117 CFS/ME patients) revealed genomic subtypes with distinct differences in SF36 scores, clinical phenotypes, severity and geographical distribution. Antibody testing for Epstein-Barr virus, enterovirus, Coxiella burnetii and parvovirus B19 revealed evidence of subtype-specific relationships for Epstein-Barr virus and enterovirus, the two most common infectious triggers of CFS/ME. CONCLUSIONS: This study confirms the involvement of these genes in CFS/ME. PMID: 19955554 [PubMed - indexed for MEDLINE]Free Article

Gulf War hero arrested by VA cops for helping fellow veteran, now is criminally harassed August 19, 2010 posted by Michael Leon · 5 Comments Glenn McBride, a 14-year veteran of the Army, received a perplexing letter from the Department of Veterans Affairs that included a request for more information about his "menstrual disorder." - VA cops continue their mindless and illegal harassment of veterans. Decorated veteran is denied honest services by federal VA employees in violation of federal statute, TITLE 18 > PART I > CHAPTER 63 > § 1346 - By Glenn McBride I embarrassed the Roanoke Virginia VARO back in April of this year, and they have been gunning for me every since. Here is the Fox News story. I went in to the Roanoke VARO on Tuesday the 17th of August 2010 and a veteran asked me for advice as he heard me talking to my friend about his VA problems. I assisted the veteran in filing a 4138 requesting a copy of his entire C&P file from the VARO. Within minutes I was arrested by 3 armed federal protective service guards and 2 level 8 VA managers. The charge was solicitation. I would appreciate the opportunity to get this into the media. If veterans are not free to speak to each other about their VA claims while on VA property, do we really have freedom of speech? By Jana Winter from Fox News Last month, a decorated Gulf War hero received a letter from the Veterans Affairs Administration that said: We are working on your claim for menstrual disorder. There was just one problem: The claim was submitted for fibromyalgia. Make that two problems: The claim was submitted by Glenn McBride, a 40-year-old man from Roanoke, Va., who most definitely does not get menstrual cramps. It’s a bad sign when your health insurance provider can’t figure out which gender reaches for the Midol. (Hint: it’s the one without the prostate.) The Department of Veterans Affairs is notorious for bungling health care benefits, and its Roanoke regional office, which handled McBride’s claim, has long been considered among the worst. In September 2009 a surprise inspection found the office was collapsing under the weight of its own bureaucratic incompetence. Literally. Its filing system — floor-to-ceiling stacks of overfilled file cabinets and loose claims folders — weighed twice as much as the building’s structure allowed, threatening the lives of everyone inside. Inspectors also found missing and improperly filed, stored and processed claims, among other problems. The regional office was ordered to overhaul the health care processing center completely. By last month, six months later, there should have been some improvement. Instead, McBride received a letter that included this perplexing request for additional information: “On the VA Form 21-4138, Statement in Support of Claim you sent on October 8, 2009, you included menstrual disorder. Please specify what you intended to claim for this condition.” Click here to see the VA’s menstrual letter. McBride, whose 14 years of Army service included a combat tour with one of the most highly decorated units during Desert Storm — and did not include any complaints about menstrual cramps, so far as he can recall — insists this was not just a clerical error. He says it’s one more example of the VA ignoring or messing up claims in order to avoid paying benefits. “If the VA does not actually recognize the request, they do not have to give the award,” he said. “Sort of like a perverted form of ‘See no evil, Hear no evil, Speak no evil.’ Most people just throw up their hands in frustration and walk away at this point. That is the VA’s plan.” The VA, asked to comment about McBride’s complaint, issued a statement in which it said: “The Department of Veterans Affairs’ (VA) mission is to be an advocate for Veterans. VA has a responsibility to assist Veterans during the claims process. Part of that duty is to include all possible issues that a Veteran references in his or her initial claim package. VA regrets any confusion that Mr. McBride’s claim may have caused. VA Regional Office employees have reached out to Mr. McBride to clarify the confusion, determine the types of issues he wants to claim, and identify any outstanding concerns that he may have.” Jim Strickland, a veterans advocate who writes a regular health care benefits column on VAWatchdog.org and has his own benefits-related Web site, said he wasn’t at all surprised to learn of McBride’s “menstrual” letter. “There are 57 regional offices and every one is operating in total chaos and in crisis,” he said. “Full frontal mass chaos. Every day.” Contacted in the middle of the week, Strickland said he’d already received two e-mails from veterans who were mailed the records of other veterans. And he provided his most ridiculous example of a nonsensical claims letter, one that managed to try to collect debt and to discuss overpaying the same debt — at the same time. For Gulf War veterans who fought during a certain time period, certain health conditions are considered presumptive, meaning that such a high percentage of that group has been diagnosed with the condition it’s presumed that it was caused by military service, and coverage is automatically granted. Fibromyalgia, a chronic pain condition, is a presumptive one for McBride. Because of his years of experience dealing with the VA, McBride likes to provide as much information as possible when he submits claim forms. (He also gets a signed and time-stamped receipt upon delivery.) When he sent in his claim for fibromyalgia, he typed clearly at the top of the form: “This form is an official request for SERVICE-CONNECTION for FIBROMYALGIA.” He included an extract of a VA “fast letter” regarding presumptive conditions — basically providing the VA with its own policy on Chronic Fatigue Syndrome, Fibromyalgia and Irritable Bowel Syndrome. “Menstrual disorder” is included in the VA’s list of symptoms. “The VA just breezed right through the facts and settled on the obscure,” McBride said. “The Roanoke office clearly hasn’t changed.” Strickland says the problem at the root of letters like McBride’s is a bonus structure paid out to VA claims employees. “The more work, the better the bonus is,” he said. “It’s strictly volume, not quality driven. There is no accountability whatsoever. “The art of the Teflon Jacket has been perfected at our VA. They are really totally invulnerable to your criticism.” When the editor of VAWatchdog.org posted an April Fools Day joke — “VA DOCTOR TRIES TO GIVE PROSTATE EXAM TO WOMAN VETERAN (April Fool); VA physician: ‘Nobody told me the patient was a female. How the hell was I supposed to know that?’” — McBride sent in his “menstrual” letter. It was posted on the same site under the heading, “Today’s Whiskey Tango Foxtrot? award goes to the VA’s Roanoke, Virginia Regional Office.” The site’s editor describes the award: “Every now and then we get a story about the VA that just can’t be. But, it is! Because, remember, we’re not dealing with regular people … we’re dealing with the VA. That’s when we throw up our hands and scream at the sky: “‘Whiskey Tango Foxtrot?’” Which is longhand for: WTF.

LINK FOUND BETWEEN REPEATED HEAD INJURIES AND LOU GEHRIG'S DISEASE Repeated concussions may contribute to the development of symptoms that mimic amyotrophic lateral sclerosis, or Lou Gehrig's disease. NOTE from Larry Scott, VA Watchdog dot Org ... In 2008, VA established ALS as a presumptive compensable illness for all Veterans with 90 days or more of continuously active service in the military. The VA had a hand in this research and their press release is here ... http://www.vawatchdo...vap081910-2.htm For more about veterans and ALS, use our search engine ... here ... http://www.yourvaben...hp?q=als&op=and ------------------------- Link found between concussions and Lou Gehrig's disease Melissa Healy, Los Angeles Times Staff Writer http://articles.latimes.com/2010/aug/17/new s/la-heb-brain-trauma-20100817 Repeated concussions may contribute to the development of symptoms that mimic amyotrophic lateral sclerosis, or Lou Gehrig's disease, a controversial group of researchers is suggesting in a provocative new study. The cause of most cases of ALS--a devastating degenerative disease named after the baseball great who was its most famous victim--is largely a mystery. Only 5% to 10% of those who are diagnosed with ALS carry the distinctive gene mutation known to give rise to the disease: Of the 30,000 Americans who have the disease at any given time, at least 27,000 have no clue as to its origins. The study suggests that the symptoms that felled baseball's beloved "Iron Horse"--spastic movements, muscle weakness and progressive loss of muscle control--may, in part, have been the result of his legendary penchant for playing while injured, including after concussion. The suggestion that traumatic brain injuries--also called concussions--may contribute to neurodegenerative disease is not new. But a growing body of research has strengthened evidence that concussion may be the catalyst for a wide range of brain diseases, from depression and dementia to Parkinson's disease symptoms and now, movement disorders such as ALS. Dr. Martina Wiedau-Pazos, an expert in movement disorders at UCLA who was not involved with the latest study, called the study's findings "very intriguing," but cautioned that the study was too small to allow clinicians to draw broad conclusions about the prevention or diagnosis of diseases like ALS. Neurobiologist Donald Stein of Emory University, who studies concussion, said the study's authors have raised the possibility that some patients with past brain trauma who appear to have ALS may have another disorder altogether, which may progress differently, and respond to different therapies, than ALS. "It's very impressive to me," said Stein. The latest article recounts the first pathology study to find similarities between a concussion-related brain abnormality and abnormalities in the brains of patients with degenerative disease that affects the brain regions responsible for movement. It compares the autopsy slides and samples of 12 professional athletes' brains and spinal cords with those of 12 patients, matched for sex and age, who had died with a diagnosis of ALS, and another 12 patients who were free of brain disease at the time of their death. All of the athletes whose remains were studied had suffered repeated concussions in their playing years, and suffered from chronic traumatic encephalopathy, in which the same kinds of tangles as are found in Alzheimer;'s disease patients appear throughout the brain. In the case of all but one of the athletes studied, remains had been donated to Boston University's Center for the Study of Traumatic Encephalopathy. The study found distinctive protein abnormalities in the brains and spinal cords of three of the athletes who, in addition to traumatic encephalopathy, had developed motor symptoms that were diagnosed as ALS. The same array of distinctive abnormalities was found in the brains of all of the patients who had died of ALS, and none of those who had died with intact brain function. "The play of contact sports, such as boxing, football and hockey, might be associated" with the protein abnormalities seen in the brains of the motor-impaired brain-injury victims as well as those whose impairment was the result of disease, the authors--led by Dr. Ann C. McKee-- wrote. "Whether repetitive head trauma alone provokes these neurodegenerative cascades, or only in association with certain genetic constellations remains to be determined," they added. Traumatic brain injury is often called "the silent epidemic" because in spite of the fact that 1.5 million Americans yearly are thought to suffer traumatic brain injury, the effect of such brain injuries on the nation's health--as well as that of the individuals affected-- has, until recently, been largely ignored. With as many as 360,000 U.S. troops returning from Iraq and Afghanistan having suffered a traumatic brain injury during service, that has begun to change.

I am not sure what your VFW Rep. was talking about but most likely VA will take this as a Notice of Disagreement. If you have not heard from VA, you should try to get all the information you need to support all your claims and send it in as soon as possible. If your claim was awarded in Sept. 2009, you would have until Sept. 2010 to file a NOD not 60 days. This is a NOD and a claim for increase. Have you filled out the TDIU form? If not you may want to fill it out and send it in. http://www.vba.va.gov/pubs/forms/VBA-21-8940-ARE.pdf

Congrats.

I am not familiar with your situation but keep in mind that VA has fuzzy math, according to VA 70+20+10=78 and VA rounds off and will only pay you 80%

Yes, this does happens a lot. A few years ago I was waiting on a rating decision from VA and it finally came and I opened it and started reading as fast as I could and then found out that my claim was denied. I went to the reason for decision and was reading a denial for something I didn't claim and then I look at the cover sheet and found out that it was not my claim but another veteran's claim. I called VA and told them and they sent an envelope for me to return it. I think it happens more then we could imagine.

Welcome to Hadit, you may want to try to read the CFR 38 part 4 http://ecfr.gpoaccess.gov/cgi/t/text/text-idx?c=ecfr&rgn=div5&view=text&node=38:1.0.1.1.5&idno=38 It is what VA uses to rate all claims. It is a lot to read but it is a start. If the site does not open, just close the site and try it again. It does work but it likes to be difficult at times. I won all my claims just reading the CFR 38 Part 4 but I still have claims pending. I did have some help from a few service officers but decided to work on the rest of my claims myself. You can always get a service officer to help you file your claims or you can get the help and direction you need from Hadit.com If you can get a statement from your doctor that states that your knee injury cause your back problems then you can file a claim for back condition secondary to your already service connected knee condition. The doctor must review your military records and private records then write a statement that she or he has reviewed your military and private records and it is her or his medical opinion that your knee condition most likely caused your back condition. You must also have a current diagnosis of your back condition. Others will chime in.

Gulf War Veterans Show Illness Is Real in Airway Studies August 17, 2010 posted by Denise Nichols · Ill Gulf War Veterans Show Sleep Disorder Breathing A new study of Gulf War illness has been reported. The study shows sleep disordered breathing for ill gulf war veterans. Eighteen ill gulf war veterans and eleven non-ill gulf war veterans were used. The results showed increased frequency of arousals related to apneas, hypopneas, and mild inspiratory airflow limitation results. So more studies are showing this is a real problem not just psychological! Abstract Purpose To determine whether veterans with Gulf War Illness (GWI) are distinguished by sleep-disordered breathing, we compared inspiratory airflow dynamics during sleep between veterans with GWI and asymptomatic veterans of the first Gulf War. Methods We recruited 18 male veterans with GWI and 11 asymptomatic male veterans of the first Gulf War by advertisement. The two samples were matched for age and body mass index. Each participant underwent a first full-night polysomnogram (PSG) while sleeping supine using standard clinical monitoring of sleep and breathing. A second PSG was performed measuring airflow with a pneumotachograph in series with a nasal mask and respiratory effort with a supraglottic pressure (Psg) catheter to assess the presence of inspiratory airflow limitation during supine N2 sleep. We determined the prevalence of flow-limited breaths by sampling continuous N2 sleep and plotting inspiratory flow against Psg for each breath in the sample. We expressed the prevalence of flow-limited breaths as their percentage in the sample. Results Compared to controls, veterans with GWI had an increased frequency of arousals related to apneas, hypopneas, and mild inspiratory airflow limitation. During supine N2 sleep, veterans with GWI had 96 ± 5% (mean ± SD) of their breaths flow-limited while controls had 36 ± 25% of their breaths flow limited (p < 0.0001). Conclusions Veterans with GWI experience sleep-disordered breathing that may distinguish them from asymptomatic veterans of the first Gulf War. http://www.veteranst...airway-studies/

Congrats

Congrats

Congrats