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Everything posted by Buster

  1. Sorry, I don't have it automatically updating, I have to cut and paste between two web sites. I'm still seeing if there is another way to do this, but we're up to 87 people.
  2. Dr. K certainly would say so. I'd imagine that as long as it is self-reported, that will be true.
  3. In the classic way of social network, can I ask folks to PM others who they know of but aren't on the map? I'd love to get as many cases up here. Not sure what we'll do with the data yet -- and you might have to do this again once we figure out the map. I don't have a way to automate survey monkey to geomaps but will keep the two synchronized as often as possible. There's another tool I might use that enables a shared map -- investigating now. Buster
  4. PITAND is fine. I purposefully avoided asking about Strep. Please mark whether symptoms were dramatic onset or not. I probably also should have asked about OCD vs Tics -- so I may have to start another survey. Please keep suggestions coming here and I'll make another of these as I figure out what I should have asked. I started plotting against population density (i.e., case per 1M people). Terribly annecdotal at the moment but based on zip codes seems currently tied to population density. I'll post more later as more data comes in (I hope). We're at 40 responses. Buster Hi Buster, Do you want PITAND also or only PANDAS? We were diagnosed as pandas but now suspect PITAND. Waiting for tests.
  5. Here's the map of cases so far. If you need to report on more than one child, please clear your internet cache and take the survey again. In terms of Zip code, please use where the child was when symptom onset was noticed. Best regards, Buster Take a look at http://www.batchgeo.com/map/3f7a8d7e9f08f58fc7469ca4689f33fd
  6. Good point, I was just trying to see where people were. Maybe I'll drop "definite" or make it into very, very likely :-) My real goal here is to try to plot those that are likely or higher on a map. Buster Hi Buster, I find it hard to answer question no. 3 : "How sure are you your child has PANDAS". Am I to choose "Definite (IVIG seemed to cure)", if I (and the doctors) am absolutely sure, that my child has PANDAS, but don´t believe or experience, that IVIG is a permanent cure ? Or am I to choose "Very Likely ..." given the above mentioned ? Couldn´t/shouldn´t it be possible to answer : "Definite (has had all clinical symptoms during PANDASexacerbations (and have periods without symptoms between PANDASexacerbations), prednisone burst and antibiotics are allways effective, IVIG brings remission, however my child has new PANDASexacerbations whenever he is infected or even exposed to strep (and/or other bacterias and vira) even after IVIG" ?
  7. In the case of our dd9, she has had difficulty copying. The word could literally be written in the question above or many times on the sheet of paper (or in the room) and she can't copy it right in the answer. She reads at an extraordinary rate with excellent comprehension, but spelling has been torture. She sight reads, but spell phonetically. She can't, however, remember which phoneme choice goes in the space. She doesn't "see" the shape. The tests isolated that an area known as her orthographic memory (i.e., spatial memory) was not functioning normally. If you use a peg board, she can get a pattern. If you ask her to copy a pattern, she couldn't. It was literally the combination of see, remember, write -- if you removed any of the steps then she could typically do the action. The easiest way to tell the difference is with our youngest daughter, when she wants to know how to spell a word, she'd like us to write it out for her. With out oldest, she wants us to tell it to her. If we write it out, it is of almost no help. For the longest time we thought this a form of dyslexia and it might be -- but it has a rather odd manifestation. Buster
  8. Hi folks, Please take a moment to answer 4 questions on this survey monkey. My goal is to try to plot a map. http://www.surveymonkey.com/s/V96RVXT This should take < 1 minute to complete. Please use zip code where you were when your child first exhibited symptoms. If you aren't in the US, please provide city/country. This isn't yet automated -- so refresh won't be immediate I'll see if there is a way to maintain a shared map once this version is done. Buster Current results for 163 responses are at http://www.batchgeo.com/map/ca5449d55ccb94010dd9dbfbc0fdd870
  9. Such a great clear question and I don't have a great answer. This may be a good one to challenge the researchers with. Let me split the question into one about other bacterial/viral infections and one about auto-feedback due to neuronal exposure. In your reading you've probably run across the term super-antigens. The exotoxins of GABHS and Staph are the best characterized super-antigens, but any pathogenic microbes can produce super-antigens (for example, mycoplasma pneuomonia). Super-antigens work by activating T-cells and recently appear to activate B-cells (http://www.springerlink.com/content/l40373ph04460474/) without any of the normal pattern matching that would activate only those antibodies for a particular antigen. This means stuff that shouldn't be getting activated is getting activated by some other trigger. I think this is explaining why mycoplasma pneumonia could be a subsequent trigger. I even wonder if this is what is happening in Lyme. Now the other part of your question is much more tricky. If a T-cell finds neuronal tissue, will it activate a B-cell and create the 24.3.1 antibody. This makes sense to me but frankly I don't know. ADEM could easily be this situation (i.e., an activated B-cell that producing antibodies that actually signal destruction of neuronal tissue). In ADEM, they see the white patches on MRIs indicating demylination and so my gut says that ADEM is a BBB disruption that triggers antibodies that cause destruction of neuronal tissue. I don't think this is the case in PANDAS because they don't see demyelination. In PANDAS, they don't see those white patches. By the way, that actually is good news. It's as if the antibodies are binding to the dopamine/tubulin receptors but not triggering phagocytosis (i.e., interference without causing macrophages engulfment or cell apoptosis). This makes me think it is more a super-antigen recruitment of non-specific T-cells rather than a straight feedback cycle of an open BBB causing B-cells to trigger anti-neuronal antibodies. I hope the above makes sense. I should stress that I don't think anyone knows. What's interesting in PANDAS is that it looks like binding is occuring but not destruction -- interference rather than demyelination. Regards, Buster Peg - yes - thank you - that is EXACTLY what I was trying to say! You are so articulate~!
  10. All antibiotics carry some concerns here, the exact text for clarithromycin reads "Hepatic dysfunction, including increased liver enzymes, and hepatocellular and/or cholestatic hepatitis, with or without jaundice, has been infrquesntly reported with clarithromycin. This hepatic dysfunction may be severe and is usually reversible." Buster
  11. Hi Suzan, PANDAS is thought to be due to an auto-immune response and not due to strep antigens crossing the BBB. Antibodies have (in general) a 28 day half life. This means that once the trigger is gone, the antibodies go down by 1/2 in 28 days then are about 1/4th as strong in 56 days and then 1/8th as strong in 84 days etc. The exact half-life isn't perfectly known but it looks like 28 days is about right. Okay, so what you really have are three independent events: an abnormal immune response to a bacterial infection triggering B-cells to produce anti-neuronal antibodies a failure to "recognize self" and suppress the anti-neuronal antibodies a breach in the BBB that allows the anti-neuronal antibodies to reach the neuronal tissue So assume you get the BBB closed, well the antibodies will keep circulating for typically 3 months. Another opening of the BBB during that time would start the whole cycle again. Remember that antibodies continue to generate as long as the target is found -- this is why auto-immune diseases are so problematic. The BBB can be breached a number of ways. High stress can cause a breach. An infection can cause a breach. Even high epinephrine can trigger a breach. Then you wait around till *both* the infection or issue keeping the BBB open is treated, the BBB closes, and the antibodies dissipate that have already crossed *and* you don't get another trigger. Hope that helps as an explanation, Buster
  12. I know exactly this feeling and this was a topic of considerable discussion in our family both before, during and after IVIG. This disease is a funny disease -- full of self-doubt for parents, hoping we're making the right choices. The notion of exposing our child to potentially an unknown virus or disease from the blood product (IVIG) caused significant concerns. Post IVIG -- especially the first 2 weeks -- we really wondered if we did the right things. The symptoms were terrible afterwards. Despite knowing that this could happen, we weren't really mentally prepared for it (okay, I wasn't -- dw says she was). It really made us wonder whether we had made the right choice. Then week 3 came along and everything got way better and then 6 months of calm. I'm sure some doctor will say that it was all a coincident, but frankly 1 month post IVIG was when I really understood how bad things had been and was so grateful for the decision we made. Bottom line, line up your support folks -- make sure you and your spouse are well aligned -- get a few of us on the board in your fast PMs. Be prepared that doubt will creep in, but you've done all the research, you are following the best advice possible, IVIG is well tolerated by most and although there is exposure -- the risk benefit analysis is really where you should focus. If you've got good clinical evidence for PANDAS, if the symptoms are getting bad enough you don't see antibiotics or other things improving situation, then IVIG is the discussion point. At least at the moment you have the option. Wishing you the best, Buster
  13. Hi, not quite sure how to give advice here. You do need a doctor you trust to be your primary advisor. In general, a 5 day prednisone treatment is used by many doctors as a diagnostic tool and not as therapy. This means that symptoms that are auto-immune or due to inflammation generally return post burst. There are some studies that longer pred does bring some relief in other ailments, but the use of pred is not well studied for PANDAS. Biaxin (Clarithromycin) is a very good antibiotic but there are some concerns of liver or kidney damage with long term use. Biaxin has excellent penetration and in most patients is effective at a wide range of bacterial infections (particularly skin infections). Most on this forum are on either Azith or Augmentin, but again you really will need a pediatric or immunologist to advise you here. It's great you've had symptom remission. Regards, Buster
  14. Can't say we've tried that, but we have noticed increased exacerbations around time of seasonal allergies. In addition, our daughter tends to be a histamine cascader -- i.e., she gets itchy when she runs. There's probably something in this (i.e., some inflammation due to allergy too). I haven't found any great research on this yet though. Buster
  15. I was going over the current FAQ to see if there were things missing that should be added in. http://www.latitudes.org/forums/index.php?showtopic=6266 Anyone have questions that have come up over past few months that we need to roll in. Some I've seen have been: 1) Why do I see exacerbations with illnesses other than GABHS? 2) What is the accuracy of a strep throat culture (rapid or AGAR)? 3) Is blood work more accurate than a throat culture? 4) If there's no ASO rise, is there still an anti-neuronal antibody rise? 5) What's the difference between colonization and infection? Why does it matter? 6) Is there a good way to chart symptoms to make it easier to be objective? Others? Buster
  16. We had upside down behavior where our dd7 (at the time) needed to be standing on her head all the time. In our case the psychiatrist thought it was a side effect of Lexapro -- something called akathesia. She dropped her off Lexapro (which had all sorts of withdrawl symptoms) and shifted her to an alternate SSRI at a much lower dose. Sure enough, once off the Lexapro, she didn't have to be upside anymore. She could never describe why she had to be upside down. So if you are on Lexapro or an SSRI, might be something to talk to your doctor about. Buster
  17. Information on how IVIG might work http://www.latitudes.org/forums/index.php?showtopic=7855
  18. I wish for that too, unfortunately, hasn't happened yet. Unfortunately IVIG is just too broad a treatment to know what it is exactly doing. Plasmapheresis is much better understood, but it is primarily a filtering process that reduces the concentration of antibodies. If there is still an antigen, then the antibodies will likely return. With IVIG, it's more complicated and less understood. It's not clear whether the IVIG is adding back regulation (i.e., suppressing antibody binding), whether IVIG is exhausting T-cell recruitment, whether IVIG inhibits superantigens, is tagging the bacterial antigen for phagocytosis, or whether IVIG is suppressing cytokines, .... They really truly don't quite know what is happening in IVIG. For other diseases, auto-antibodies turn over (i.e., have a half-life) of about 21-28 days. This means that in the absense of a trigger about 75% of the antibodies should be gone by 6 weeks. If this is what happened in your child, then PEX (or IVIG) won't dramatically change the antibody numbers. PEX can more quickly reduce antibodies, but only if almost immediately after the antigen has been removed. If the reason the symptoms have stopped is that the blood brain barrier closed, then it's possible the antibodies are still circulating but not crossing the BBB. PEX could potentially help, but if the antigen is removed, then the antibodies would turn over on their own (given time). If the Antigen is still there, then PEX won't be a long term treatment. IVIG might (please note the underscore) help tag a bacterial antigen if it is still active and thereby help the immune system find and destroy a bacterial antigen. However, this is again a really brute force way to clear an infection. I wish we had the stone tablet. Buster
  19. Wow, tough question. The problem is that if you aren't in an exacerbation, then it's harder for the doctor to justify IVIG to the insurance as necessary -- and more importantly, it's hard for the doctor to show efficacy (in case you would need it again). In addition, there are some risks with IVIG so if you seem in a good spot, I wouldn't mess with it. While I think alot about the comment of the other post "we want to win the war not just get a truce." I think it's a lot easier to recruit all the support when the enemy attacks and harder to get justification during the truce. For what it's worth, continue going for the approval -- you don't have to use it if you get approved, but having it approved is half the battle. You can then refer to the approval later if you need it -- or provide even stronger evidence later if an exacerbation occurs. So my recommendation, keep going for the approval based on prior exacerbations, but don't use it unless you're in an exacerbation. I say this because everyone feels justified when there is noticable improvement. Everyone feels some doubt when the child is either appearing well, or there's no noticable improvement. Buster
  20. Yes. I'll probably sound like a broken record after a while (does anyone still use that expression anymore? ) PANDAS (like SC) is thought to be caused by 3 things a genetic predisposition to an unusual immune response the production of anti-neuronal antibodies a breach of the blood-brain barrier that allows the antibody to reach neuronal tissue So prednisone is affecting #2 (by immunosuppressing the production of more antibodies) and #3 (by being highly antiinflammatory). I personally think that once the BBB is open there is sort of a feedback loop that keeps the antibody production going, so closing the BBB causes a break in the cycle (no research report here, just makes sense to me). Buster
  21. In our case, we had essentially 6 months until our daughter had a fever and with a rapid return of many of the symptoms. This was despite staying on antibiotics. It was not clear to us whether the fever was due to a bacterial or viral infection. The symptoms were not as bad as the chaos that started the whole mess (probably 60% of the worst). We waited a month in hopes that the normal pattern of the exacerbation that we had observed pre-IVIG (i.e., 2 week ramp, 1 week plateau, 4-5 week fall) would happen. We had the ramp, the plateau and the fall, but the baseline did not return to the pre-fever (post-IVIG) point -- i.e., we had a baseline change. I know, not the best news, but that's what happened in our case. We had 6 months of calm and things are settling, but we're not back to "normal". Buster
  22. There's mixed studies on actual inflammation. Giedd in 2000 found that there were volumetric changes in children with PANDAS (see http://ajp.psychiatryonline.org/cgi/reprint/157/2/281) Dale had an excellent summary in http://protoc.incubadora.fapesp.br/portal/...%2072%20195.pdf There have been criticisms of this work (i.e., lack of blinding, statistical power issues, etc) but frankly the results haven't been refuted. However, Kirvan and Cunningham in 2006 started investigating another effect which was that the antibody seemed to bind to the dopamine receptors rather than causing inflammation. So what they think is going on is inflammation is happening to the BBB -- allowing the antibodies to cross. But then once across, the antibodies are binding to receptors on the basal ganglia but not necessarily causing demylination or T-cell attacks. It's really hard to tell, but frankly I feel somehow better with binding rather than "attack". Certainly the lack of leisions as seem in ADEM, gives some comfort that the effect is reversable. Unfortunately, more research needed to see. Buster
  23. Oops Thanks for the correction. Not sure how this ties to this thread, but SID is usually raised in this forum as Specific Immune Deficiency -- a failure to have IgG response to a specific antigen such as pneumonococcal antibodies. Buster
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