Objee

Josephine, When I reopened my claim at Oakland VARO, they had to retrieve the file(s) from a dead storage site in a nearby town. The claim had been "final" for 10 years. Getting the old c files to the RO took about a month. The RO had kept nothing from my decided claim - it was all sent to storage. Ralph

Romad, I talked with an eye MD friend and here's what he said: If you have Horner's, you may show a drooping upper eyelid, dry facial skin and have excessive tearing, etc. Pupils may not adjust as fast as normal. From what he said (and I'm no MD!!) rating could fall under 6009 or 6019, or both. Looks like a 10%er if not rated as part of the cluster migraines. Apparently this is nerve damage in a nerve bundle going from the hypothalamus (central brain) down to the chest, then up by the carotid artery into the inner ear, then to the eye. Whew! He said there are 3 areas in which the damage could occur and the docs can usually test to see where the actual damage is. Hope this helps - not sure I understand all of it, Ralph

Horners syndrome is actually an ocular problem: "Common causes of post-ganglionic Horner's syndrome include trauma, CLUSTER MIGRAINE HEADACHE and neck or thyroid surgery. The diagnosis and the localization of a Horner's syndrome is accomplished with pharmacological testing. Ten percent liquid cocaine (topically applied), works as an indirect acting sympathomimetic agent by inhibiting the re-uptake of norepinephrine at the nerve ending. A Horner's pupil will dilate poorly because of the absence of endogenous norepinephrine at the nerve ending. The test should be evaluated thirty minutes after the instillation of the drops to ensure accuracy. The cocaine test is used to confirm or deny the presence of a Horner's syndrome. However, a positive cocaine test does not localize the lesion. " How does Horners affect your vision/eyes? If at all, Horners is secondary to cluster migraines and should be eligible for a separate rating as secondary to the migraines. Ralph

Berta, did you get a dated, receipted copy of the IMO when you submitted it/them? I got the same lost treasure crap once, faxed them the first page with receipt stamp and their eyes got good enough to find the hopelessly lost file in one day.

Yep and it's a trial not to create something else to sumit. I guess you get a hobby and put the 800 number on your redial. Ralph

Gotta apologize for the scientific stuff in this but I can't get rid of it . . . If anybody needs the internet medical sources and more info, just let me know. Agent Orange (Dioxin) and thyroid-based/diabetic problems John C. Lowe, M.D. (N.B. The terms T 4, T3 and T2 refer to normal thyroid hormones) "Transthyretin is the protein that transports T4 across the blood-brain barrier. It also transports T3 across. It may transport less, however, because the binding affinity of the receptors within the protein is about ten times less for T3 than for T4. Nonetheless, this protein does indeed transport T3 and T2 into the brain across the blood-brain barrier. However, T3 also enters the brain, at least in mice, without riding in on transthyretin. Transthyretin also transports chemical contaminants such as dioxins and PCBs across the blood-brain barrier. The latter chemicals displace T4 and T3 from the thyroid hormone receptors inside the transthyretin molecule. Since Vietnam veterans (et al) are potentially quite polluted with these contaminants, the displacement of T4 and T3 may be a major mechanism of health problems from a brain deficiency of thyroid hormone. The potential health problems from this displacement are highly complex. In The Metabolic Treatment of Fibromyalgia *, I wrote an extensive section on the topic. In the section, I noted that after contaminants displace T4 and T3 from transthyretin, bind to the hormone receptors in the protein, and then ride the protein into the brain, the contaminants can bind to thyroid hormone receptors on genes. The binding alters the normal transcription activities of the genes, producing adverse effects that are hard to predict and diagnose.” * The Metabolic Treatment of Fibromyalgia is widely considered the most authoritative book ever published on fibromyalgia, hypothyroidism, and thyroid hormone resistance. Written by Dr. John C. Lowe in 2000 and published by McDowell Publishing. A diabetes - hypothyroidism connection Hypothyroidism is accompanied by a variety of abnormalities in plasma lipid metabolism, including elevated triglyceride and low-density lipoprotein (LDL) cholesterol concentrations. Even subclinical (not obvious) hypothyroidism can exacerbate the coexisting dyslipidemia commonly found in type 2 diabetes and further increase the risk of cardiovascular diseases. Adequate thyroxine replacement will reverse the lipid abnormalities. The hypothalamus is a small organ at the base of the brain. Metabolically, there is a thyroid and insulin connection through the hypothalamo-pituitary-thyroid axis, From an experiment published in Endocrinology. 1977 Jun;100(6):1604-9: Studies of hypothalamic and regional brain TRH# content in the rat after administration of various hormonal and pharmacologic agents were performed. No consistent changes in TRH content in the hypothalamus or brain followed thyroidectomy, hypophysectomy or administration of thyroxine or dexamethasone. There was a significant fall in hypothalamic forebrain and brain stem TRH content 60 min after insulin administration. . . And from a French experiment: Conclusion: Our present data showing that glucose stimulates and insulin inhibits pancreatic TRH release are compatible with the possibility that this substance may play a role in glucoregulation. # TRH = Thyrotropin Releasing Hormone (a thyroid stimulating hormone.) (Those BS spikes you sometimes see don't only directly affect diabetic stress, they can cause amplified reactions through other metabolic paths!) WHat the above points out is that not all Type II diabetic problems are limited to the diabetes - thyroid failures can make diabetic symptoms worse. Ralph

Cavman, I had the same result with my NoD when the RO carved 2 "new" claims out of the NoD and said they would decide these first, then the remaining NoD claim. The NoD included a response to "deemed denied" claims which were the ones the VA said were new. Screws the whole situation up on decision timing and will probably cause a new NoD for the "new" claims to get an EED. Ralph

https://iris.va.gov "ASK A QUESTION"

I've got good enough relations with my VA treating physicians that they ask me to draft their opinion letters (after we discuss what I need.) I tail their opinions with a paragraph starting "My opinion is further supported by information in the body of medical knowledge such as" [quotes from PUBMED, NIH, etc.) This makes the internet info a medical instead of lay submission. My VSO says this will help internet evidence submision credibility. Sure hope so! Ralph

I had thyroid papillary cancer caused by ionizing radiation, but looked at AO/dioxin as a cause too. Evidence isn't strong, but there is some pointing to dioxin as a thyroid cancer cause, at least in lab animals. The experiment following showed a significant increase in both liver and thyroid cancer in lab rats exposed to elevated levels of dioxin: Kociba RJ, Keyes DG, Beyer JE, et al. 1978. Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-TCDD in rats. Published in Toxicol Appl Pharmacol 46:281-287 Research will at least give you medical information pointing at a possible dioxin/thyroid connection. Everything like this that you can find is initial medical evidence, until you can find an MD who will write about a possible connection. Good luck, Ralph

I've only submitted 1 IMO for my multiple claims. Everything else has been through VA doctors. Up until (I think) September 2005, there was VHA Directive 2000-029 that authorized VA docs to write medical opinions for vet claimants. I have heard, but not been able to verify, that this directive has been extended past 9/2005. I did all the research, reviewed my medical records and wrote sample letters for each doc. Gotta use the right medical terminology. Each MD read the letter(s) and was willing to discuss them with me. In 2 cases, they added to my writeup and corrected some errors, making the opinions even stronger than I wrote. I would never ignore your VA docs, particularly if you've cultivated good relations with them. Ralph

Rigo, Thanks for the great example. I listed the "deemed denied" claims in my NOD and VARO responded with an acknowledgement of the 2 deemed-denied claims as new claims. I expect at least one of the "new" claims to be granted. How do you suggest I NOD for an EED back to the original filing they ignored for these 2 claims? I'm a bit confused if this is different from your example or not. Ralph

Rigo, Thanks for the great example. I listed the "deemed denied" claims in my NOD and VARO responded with an acknowledgement of the 2 deemed-denied claims as new claims. I expect at least one of the "new" claims to be granted. How do you suggest I NOD for an EED back to the original filing they ignored for these 2 claims? I'm a bit confused if this is different from your example or not. Ralph

Don't know if this connects in the right direction or not, but check this out: COPYRIGHT © 2006 by the American College of Chest Physicians. Sleep Apnea: Treatment Options and Comorbid Outcomes Tuesday, October 24, 2006 12:30 PM - 2:00 PM THE ASSOCIATION BETWEEN OBSTRUCTIVE SLEEP APNEA SYNDROME AND THE COMPLICATIONS OF DIABETES MELLITUS Semaan G. Kosseifi, MD*, Alan Peiris, MD, PhD, Beth Bailey, MD, PhD, Robert Price, PhD, Thomas M. Roy, MD, FCCP and Ryland P. Byrd, MD, FCCP James H. Quillen College of Medicine, Johnson City, TN PURPOSE: Obstructive sleep apnea syndrome (OSAS) and diabetes mellitus (DM) are commonly encountered diseases, each associated with a substantial risk of morbidity and mortality. Recent evidence suggests that the presence of OSAS may increase the risk of developing insulin resistance and type 2 DM. The purpose of this study was to test our hypothesis, that OSAS and DM complications are related. METHODS: The electronic charts of all DM patients referred for sleep studies over a one year period were reviewed. Data collected included patient's age and gender, body mass index, glycosylated hemoglobin A1c (HgA1c), evidence of microalbuminuria, presence of microvascular complications (retinopathy and/or neuropathy), presence of macrovascular complications (coronary artery disease, carotid disease, stroke or transient ischemic attack) and multiple OSAS variables produced by sleep study. Analysis involved examining bivariate associations between OSAS variables and metabolic syndrome parameters. RESULTS: From a total number of 447 patients who over one year period, 127 patients with DM were identified. AHI (Apnea Hypopnea Index) was directly related to diabetic microvascular complications (p <0.05) and macrovascular complications (p <0.1). The number of hypopneas was also direclty related to microalbuminuria (p <0.1). The number of apneas was significantly related to macrovascular (p <0.1) and microvascular complications (p <0.05). Oxygen saturation was significantly inversely related to microalbumin (p< 0.01), macrovascular complications (p <0.1) and microvascular complications (p <0.05). The average HgA1c in our study group was significantly below the national HgA1c average. HgA1c was not associated with any of the sleep parameters. CONCLUSION: Despite well controlled DM, as reflected in HgA1c, OSAS was directly related to microalbuminuria, microvascular and macrovascular complications. Although OSAS and type II DM are independent diseases, our study support the hypothesis that OSAS may contribute to DM complications. CLINICAL IMPLICATIONS: Screening diabetic patients for OSAS should be thought about early on in the work up and management of such population since this might be a potentially treatable cardiovascular risk factor.

New system tracks Agent Orange exposure in Vietnam Between 1961 and 1971 U.S. military forces in Vietnam dispersed more than 19 million gallons of herbicidal agents, including more than 12 million gallons of Agent Orange. A large number of the American men and women who fought in the Vietnam War were exposed, but the health effects still are not fully known. Now, as part of a study at Columbia University's Mailman School of Public Health (MSPH), researchers have developed a geographic information system to accurately estimate these exposures—analyzing the relationships among herbicide spraying, geography, population, and troop location. The study, led by Dr Jeanne M. Stellman, professor of clinical health policy and management at MSPH, and Dr. Steven D. Stellman, professor of clinical epidemiology at MSPH, was published in the March issue of Environmental Health Perspectives. For more information or to obtain a copy of the abstract, contact Stephanie Berger at 212-305-4372 or sb2247@columbia.edu.

Sorry, I couldn't find the article source. There's a lot on the internet about sleep apnea and hypertension. Here's an article from the New England Journal of Medicine: Volume 342:1378-1384 May 11, 2000 Number 19 Prospective Study of the Association between Sleep-Disordered Breathing and Hypertension Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D. ABSTRACT Background Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies. We performed a prospective, population-based study of the association between objectively measured sleep-disordered breathing and hypertension (defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications). Methods We analyzed data on sleep-disordered breathing, blood pressure, habitus, and health history at base line and after four years of follow-up in 709 participants of the Wisconsin Sleep Cohort Study (and after eight years of follow-up in the case of 184 of these participants). Participants were assessed overnight by 18-channel polysomnography for sleep-disordered breathing, as defined by the apnea–hypopnea index (the number of episodes of apnea and hypopnea per hour of sleep). The odds ratios for the presence of hypertension at the four-year follow-up study according to the apnea–hypopnea index at base line were estimated after adjustment for base-line hypertension status, body-mass index, neck and waist circumference, age, sex, and weekly use of alcohol and cigarettes. Results Relative to the reference category of an apnea–hypopnea index of 0 events per hour at base line, the odds ratios for the presence of hypertension at follow-up were 1.42 (95 percent confidence interval, 1.13 to 1.78) with an apnea–hypopnea index of 0.1 to 4.9 events per hour at base line as compared with none, 2.03 (95 percent confidence interval, 1.29 to 3.17) with an apnea–hypopnea index of 5.0 to 14.9 events per hour, and 2.89 (95 percent confidence interval, 1.46 to 5.64) with an apnea–hypopnea index of 15.0 or more events per hour. Conclusions We found a dose–response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors. The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population. Source Information From the Departments of Preventive Medicine (P.E.P., T.Y., M.P.), Medicine (J.S.), and Biostatistics and Medical Informatics (M.P.), University of Wisconsin School of Medicine, Madison. Address reprint requests to Dr. Peppard at the Department of Preventive Medicine, University of Wisconsin, 502 N. Walnut St., Madison, WI 53705, or at ppeppard@facstaff.wisc.edu. As I said, there's a lot more on this on the internet. But, this is a powerful start! Ralph

Sorry, I couldn't find the article source. There's a lot on the internet about sleep apnea and hypertension. Here's an article from the New England Journal of Medicine: Volume 342:1378-1384 May 11, 2000 Number 19 Prospective Study of the Association between Sleep-Disordered Breathing and Hypertension Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D. ABSTRACT Background Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies. We performed a prospective, population-based study of the association between objectively measured sleep-disordered breathing and hypertension (defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications). Methods We analyzed data on sleep-disordered breathing, blood pressure, habitus, and health history at base line and after four years of follow-up in 709 participants of the Wisconsin Sleep Cohort Study (and after eight years of follow-up in the case of 184 of these participants). Participants were assessed overnight by 18-channel polysomnography for sleep-disordered breathing, as defined by the apnea–hypopnea index (the number of episodes of apnea and hypopnea per hour of sleep). The odds ratios for the presence of hypertension at the four-year follow-up study according to the apnea–hypopnea index at base line were estimated after adjustment for base-line hypertension status, body-mass index, neck and waist circumference, age, sex, and weekly use of alcohol and cigarettes. Results Relative to the reference category of an apnea–hypopnea index of 0 events per hour at base line, the odds ratios for the presence of hypertension at follow-up were 1.42 (95 percent confidence interval, 1.13 to 1.78) with an apnea–hypopnea index of 0.1 to 4.9 events per hour at base line as compared with none, 2.03 (95 percent confidence interval, 1.29 to 3.17) with an apnea–hypopnea index of 5.0 to 14.9 events per hour, and 2.89 (95 percent confidence interval, 1.46 to 5.64) with an apnea–hypopnea index of 15.0 or more events per hour. Conclusions We found a dose–response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors. The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population. Source Information From the Departments of Preventive Medicine (P.E.P., T.Y., M.P.), Medicine (J.S.), and Biostatistics and Medical Informatics (M.P.), University of Wisconsin School of Medicine, Madison. Address reprint requests to Dr. Peppard at the Department of Preventive Medicine, University of Wisconsin, 502 N. Walnut St., Madison, WI 53705, or at ppeppard@facstaff.wisc.edu. As I said, there's a lot more on this on the internet. But, this is a powerful start! Ralph

From BVA congressional testimony on the CVAC judges’ retirement program in 1998: Judge STANDEFER. I might just explain very briefly our organization. And that is, we're divided into four decision teams, and the four teams are: Board members and their support staffs—that is, the attorneys who help them prepare decisions; out of my office then, we have what is called a Litigation Support Unit, the two are separate—that is, the Decision Teams are separate from the Litigation Support Unit. Our General Counsel's Group 7, from time to time, in defending the Secretary of Veterans Affairs before the Court will consult with our litigation support unit seeking advice as to the best defense. We give them that advice, but that's all it is. Mr. FILNER. Wait, wait, wait—you give them advice as to their best defense? Judge STANDEFER. If they seek it. Mr. FILNER. You just made the decision, presumably negative to the party, and then you're going to be involved in advice to the attorney who now takes the case to defend the decision? Judge STANDEFER. If they seek that advice, we will give it to them based on our expertise. Mr. FILNER. I don't have enough time here right this second, but that seems to me, again, as a layman and not an attorney, that if I were a litigant here, and I knew that the folks who just made an adverse decision on me were then involved in dealing with the next level of argument, it would seem to me that I would not be getting a fair deal here. And, Mr. Chairman, I would like—I'll come back to it in another question round—but I would like to introduce in the record a packet of materials that, I assume, the later testifiers will refer to, a packet of correspondence between DAV and the VA, memos from the Litigation Support Division to the attorney for the VA. There are pages of very minute discussions of reactions to a draft decision line-by-line going over the matter. This is not just expurgating a record or presenting the record of decision. This is detailed advice. And it is put in a very disrespectful way, the first thing from your Litigation Support Division said refers to the veteran: ''Did this guy have two accidents in 1981 or did he only have one?'' - - - - - The BVA is a board, not a court. The CVAC is an Article I court, not a part of the VBA. What the hell's going on here?

Doesn't pertain to the spine, but gives an idea of favorable/unfavorable ankylosis: From BVA 9410884 - "Ankylosis is considered to be favorable when the ankylosis does not prevent flexion of the tip of the finger to within 2 inches (5.1 cm) of the median transverse fold of the palm. It is unfavorable when it precludes such motion." Guess you'll have to find out the exact motion range for favorable/unfavorable spinal ankylosis.

I don't think we're powerless. I think we're disorganized! If we could get a cohesive group of veterans together nationally, get media publicity and conduct an ongoing protest movement emphasizing the effects of past VA practices on today's returning Afghanistan and Iraq service men and women and soon-to-be vets, we could probably become a deciding force for the 2008 election! And if we could let the congresscritters know we're on track right now - we might even influence the 2006 - 2008 legislative period. Whatcha think?

Along the same lines, I'm trying to help another vet with his AO claim. This summarizes his C&P and the response I wrote for him. I need criticism from all you educated people - please! I want to help, not hurt him. Veterans Affairs Regional Office 1301 Clay St., Room 1300N Oakland, CA 94612-5209 Re: Rolf T. XXXXXX, SSN XXX-XX-6642 C&P exam of 6 SEP 06 Dear Sir or Madam: This letter is to protest that the C&P examination conducted by VAMC Martinez staff physician Dr. Thomas E. XXXXXX on 6 September 2006 is inadequate for purposes of adjudicating my claim for mycosis fungoides (MF). A number of assertions made by Dr. XXXXXX are incorrect. Dr. XXXXXX had no medical information on my condition – no C-file, no lab studies, no progress notes, no clinical diagnoses – nothing! (The claimant has no knowledge whether the RVSR at the Oakland RO furnished an exam guide and questions to be resolved or not – the so-called “blue sheet”.) I furnished Dr. XXXXXXX with my copies of the Compensation and Pension Examination guide for Lymphatic Disorders, relevant Consult Requests, and Progress Notes from VAMC San Francisco, along with write-ups of medical studies relevant to visual diagnosis of mycosis fungoides and application of the gene rearrangement studies to patch stage MF. In order of presentation in the C&P Progress Notes, here are the important errors in Dr. XXXXXX’s history, exam and assessment: HISTORY The “Doctor” YYYYYYYY mentioned herein is actually Nurse Practitioner YYYYYYY. My consult was to the VAMC San Francisco Dermatology Department and I actually see a number of other dermatology clinicians in addition to Mr. YYYYYYYY. Mr. YYYYYYY acts as the “physician of record” for some of my treatment encounters, but he also consults M.D.s on diagnosis and treatments and I see other medical staff when Mr. YYYYYYYY is unavailable. I never stated that I felt my “condition is getting somewhat better.” That question was never asked and I haven’t noticed it getting better. That’s why the UV treatment will commence now. PUVA is a recognized treatment for mycosis fungoides in the early stages. “He had a T-cell study which was performed 07/27/06 which did not support the diagnosis of mycosis fungoides” (true, but misleading – see Br J Dermatol, 2005 Aug. 153(2):368-71 below) “and therefore the acting diagnosis is psoriasis. . . . . .” (and mycosis fungoides – see VAMC Ft. Miley Progress Note of 27 JUL 06 titled “Dermatology Clinic UVL Pretreatment Assessment Note”; reference Item b) – Diagnosis). Rolf T. XXXXXX SSN: XXX-XX-6642 Page -2- “There is no working diagnosis at this point . . . .” A working diagnosis is based on a clinical impression and the treatment regimen is suited to both psoriasis and early stage MF. Progress Notes consistently mention MF history and consider it in treatment. There is no specific diagnosis of MF as yet and a C&P exam that included punch and slice biopsies would produce a result with probative value, rather than just a recap of data already clinically considered. It is mainly the lack of any consideration of relevant lab studies by the examiner that causes me to protest this C&P exam. Various Progress Notes confirm general clinical MF diagnosis agreement among dermatology staff and visiting medical personnel who had reviewed the punch and slice biopsy results. I have no protest for Dr. XXXXXXX’s exam or assessment entries as the inadequacy of the C&P exam could produce no other result. I have copied the handout given Dr. XXXXXXX relevant to specific diagnosis and the probative value of the Stanford Lab study and insert it below: “THE PROBLEM: From the PubMed of the National Institutes of Health: J Am Acad Dermatol. 2002 Dec;47(6):914-8. Mycosis fungoides: the great imitator. Zackheim HS, McCalmont TH. Department of Dermatology, University of California, San Francisco, USA. A considerable number of reports have documented mycosis fungoides (MF) mimicking other dermatoses, but a comprehensive review has not been published. Our aim was to comprehensively review reports of various dermatoses simulated by MF. Additionally, 2 cases in which MF simulated diseases not previously documented (psoriasis and erythema annulare centrifugum) are presented. A literature search of all case reports of MF cited in the MEDLINE database from 1966 through 2000 plus those in one of the author's (H. Z.) files was performed. A total of 23 reported cases of dermatoses mimicked by MF were found. With the additional 2 dermatoses now presented, this yields a total of at least 25 diseases that can be simulated by MF. In view of the considerable number of dermatoses simulated by MF, the term “the great imitator” is appropriate for MF. = = = = = = = = = = = = = = = = = = Rolf T. XXXXXX SSN: XXX-XX-6642 Page -3- THE STANFORD LAB ASSAY OF CLONALITY IS INDETERMINATE: Br J Dermatol. 2005 Aug;153(2):368-71 The usefulness of clonality for the detection of cases clinically and/or histopathologically not recognized as cutaneous T-cell lymphoma. • Alessi E, • Coggi A, • Venegoni L, • Merlo V, • Gianotti R. Institute of Dermatological Sciences, University of Milan, IRCCS Ospedale Maggiore, Via Pace 9, 20122 Milan, Italy. elvio.alessi@unimi.it BACKGROUND: The determination of clonality has proven to be a useful adjunct to the diagnosis of cutaneous lymphocytic infiltrates. It is considered particularly helpful for the distinction of mycosis fungoides (MF) and inflammatory dermatoses. OBJECTIVES: To verify the sensitivity of the polymerase chain reaction (PCR)-heteroduplex analysis of T-cell receptor gamma-chain gene (TCRgamma) rearrangements in patients with MF and to establish whether a clinicopathological re-evaluation of lesions previously unclassified or considered to be non-neoplastic entities but found to be monoclonal allowed the recognition of additional cases of MF. METHODS: Included in the study were 116 patients, seen at our Institute from April 2002 to September 2003 and tested for TCRgamma rearrangements. Thirty-six patients were affected by clinically and histopathologically proven MF, while the remaining 80 cases had not been classified or had been classified as non-neoplastic entities. The sensitivity of the molecular analysis was determined on the basis of the results obtained in the 36 patients with MF. The 29 cases of the second series of patients found to be monoclonal were clinically and histopathologically re-evaluated. RESULTS: Clonal rearrangements were found in 87.5% of patients with plaque stage MF and in 20% of those with patch stage MF. The clinicopathological re-evaluation allowed us to reclassify 15 of 29 monoclonal cases of the second series of patients as MF. CONCLUSIONS: The study showed that the PCR-heteroduplex technique can determine a high percentage of monoclonality only in plaque stage MF. However, in spite of the low sensitivity of the method, several cases previously unrecognized could be reclassified as MF when their clinical and histopathological features were re-evaluated taking into account the clonality of the lymphocytic infiltrate. Rolf T. Larsen SSN: 526-78-6642 Page -4 and final- PMID: 16086751 [PubMed - indexed for MEDLINE] Lay Analysis: This British Journal of Dermatology article reflects on the Stanford Hospital CL comment that no gamma chain was detected does not support the impression of MF. This is true, but since this Pt’s clinical diagnosis was that of patch stage MF and only 20% of patch stage Pts tested showed any clonal infiltrate rearrangements, there is no firm expectation that the assay would show clonality in a patch stage assay. Thus, this clonality testing neither affirmed nor refuted the existing clinical impression. It did, however, strongly indicate that if the Pt has MF, it has not yet advanced to the plaque stage. This comment from a website (The Doctor’s Doctor) of Paul K. Shitabata, M.D., a pathologist, bears consideration in assessing the probative value of the Stanford Lab assay: “Most cases of MF are neoplastic T helper cells which are CD4 positive. These show gene rearrangements of the T cell receptors; usually of the alpha/beta receptors, but occasionally of the gamma/delta receptors.” and “Early MF, however, is not uncommonly PCR negative for TCRG rearrangement.” Duvic M. - Cutaneous T-cell lymphoma. Program and abstracts of the 64th Annual American Academy of Dermatology; March 3-7, 2006; San Francisco, California. Discussion group 417. Further from Dr. Shitabata: “The pathologist is often faced with making the diagnosis of the early patch stage. If the classic histologic features are present associated with characteristic clinical features, the diagnosis can usually be made.” “Focal parakeratosis, sprinkling of lymphocytes in the lower layers of the epidermis, fibrosis of the papillary dermis, and scattered lymphocytes along the dermal-epidermal junction are key histopathologic features of patch stage MF.” Olsen E. - Cutaneous T-cell lymphoma. Program and abstracts of the 64th Annual American Academy of Dermatology; March 3-7, 2006; San Francisco, California. Symposium 309. I request a C&P exam for my claim that embodies the necessary punch and slice biopsies and other assessment studies required to provide the histopathologic features needed to make a specific diagnosis. Rolf T. XXXXXX Claimant ================================ Comments, Please! Ralph

The A1c study requires a blood draw and checks to see how much of your hemoglobin has sugar attached. A level of 7 to 9% glycosylation (sugar binding) is considered diabetic. The A1c checks out your BS average over time, rather than just a one-shot reading. Like a movie versus a snapshot.

I'm sure you'll get responses from those more educated than I am, but for what it's worth, here's a Statement in Support I sent in for a DRO review: "Objee" C xxx xx xxxx SLEEP APNEA CLAIM 5 OCT 2006 In addition to the VAMC Martinez records (including the physician’s nexus opinion) you have accessed, there are two more medical records in your possession needed to adjudicate this claim. They are: 1. The Final Polysomnography Report from UCSF Mount Zion Medical Center’s Sleep Disorders Center dated 27 April 1998. The sleep study was ordered by Dr. Brown of VAMC San Francisco. The study documented severe sleep apnea and bradycardia, prescribed a BiPAP set for IPAP=20cm H2O, EPAP=12cm H2O and 4L O2 and achieved a REM SAO2 nadir of 85-86% with a transcutaneous CO2 of 70-75 on the BiPAP w/4L/min. of O2. Dr. Xxxxxx’s medical opinion in the Martinez files provides the nexus to the rated radical thyroidectomy/hypothyroidism. 2. Medical summary from St. Helena Hospital, Deer Park, California covering inpatient admission from 5/28/2001 to 6/11/2001 and referencing the sleep apnea with maximum mild bradycardia most commonly occurring during the 4 AM sleep period. _____________________________________ "Objee" Claimant SInce I don't believe the DRO will look up the records, I gave a recap of the essentials I wanted him/her to know. If you list the data you submitted for heart and depression and state that you want these diseases considered, you will at the very least have made your intentions clear.

Cavman, I'm at only 10% and I just got a pair of regular glasses and a pair of reading glasses. Eye exam, prescription then a chit to fill the glasses prescription. Got them in 30 days! Objee

Patrick, Regarding the thyroid and AO - it's known that dioxin interferes with thyroid hormone action, but I don't think a direct connection between dioxin and thyroid cancer has been established with much credibility. You might look into the Collaborative on Health and the Environment in Bolinas, California. Their website is at www.healthandenvironment.org. Their website lists a strong relationship between soft tissue sarcoma and dioxin, but the relationship between dioxin and thyroid cancer specifically is weaker. The Collaborative people seem to be seriously investigating the dioxin-organ cancer relationship. Worth checking it out. Objee