Buster

There's a fair description of Choreiform movements http://books.google.com/books?id=TMupBGlpk...gue&f=false When studying choreiform movements the literature tended to refer to such movements as grimaces, shoulder movements, irregular breathing. They distinguished these from tics in that tics tended to be more regular and prescriptive. Clumsiness was often associated with choreiform movements due to an inability to sustain pressure from all fingers. Often choreiform movements finished in some other voluntary action -- more like covering up the event. So an arm twitch might end up in smoothing back hair. In our case, our daughter had a fine motor tremor, a complex measurement ritual, irregular breathing with a soft vocal tic, and an odd arm movement that resulted in needing to touch her chin with the back of her hand. We did not observe the milkmaid grip or the piano playing behavior during the height of her illness. Regards, Buster

We agree too that PANDAS and SC are part of a spectrum. When we hospitalized our daughter for her symptoms, we ran all sorts of test. Our daughter did present with elonged QT interval on her initial EKG and was left on multi-lead EKG each night for 5 days to monitor for events. The conclusion was that the elongated QT interval and significantly low blood pressure were due more to malnutrition rather than likely ARF. She had verbal tic, fine motor tremor, and debilitating OCD, but did not have the chorea or milk-maids grip typically associated with SC. She did culture positive for GABHS and was started on Augmentin that produced noticable improvement within 24 hours (albeit not complete remission). About 6 weeks later, however, she got re-exposed to strep again and her symtpoms escalated along with a significant movement disorder. We spent a significant about of time asking folks to view videos and let us know if the complex motor abnomality was an OCD compulsion (psychiatrist), mild chorea (pediatrician), a tic (neurologist) or choreiform movements. So far no heart murmurs or other indication of heart difficulties. We've read the studies by Snider that seems to indicate that PANDAS doesn't have the ARF heart issues. Regards, Buster

Kim, Way back in March of 2008, we started pursuing this route because our daughter's symptoms became severe after tooth extractions (she had to have two teeth extracted and they did them about 2 weeks apart). At the time we thought she had the rare B12 deficiency. When we tested for B12 deficiency (while doing other blood work) she came back normal. Instead we think that the tooth extraction (i.e., why she was having the Nitrous Oxide) allowed colonized strep to enter her blood stream and trigger the high antibody response. What was amazing to us was that the exacerbations were within 24 hours after extraction. I'd be interested in what tests looked for the CBS mutation. Regards, Buster

In another thread there were some discussions regarding allergies... Did anyone in their blood work while checking for Igg or other stuff have high eosinophils? Buster

Hi Judy, From your description, I was wondering if you are seeing impetigo or perhaps something more like fever blister or canker sore. Are they like these? http://www.21stcenturydental.com/smith/education/ulcers.htm. Yeast is a pain to get rid of. Numerous folks on this forum have had to address increased yeast infections and perhaps they'll add their comments regarding how to get rid of it. In our case, our daughter's OCD directly impacted her ability to eat -- but this was before antibiotics. Our daughter had a fever on Jan 23rd, 2008 and in the following week stopped eating snacks. She had a tooth extraction in Feb and after that her symptoms ramped signficantly such that she was down to eating 1 small meal per day. She had body morphology issues and all the classic symptoms of anorexia nervosa in a 7 year old. Her rationale for not eating was so that if she did eat something "she wouldn't weigh more than 50 lbs". There's a lot to our story, but the short summary is that when she was down 15% we were able to hospitalize her for malnutrition. It was there that we were able to culture her and get blood work and discovered that she had GABHS as did her sister. After Augmentin it was as if a cloud cleared and a part of her came back but it was a fight for the next 3 months as the symptoms came back when we switched from Augmentin to Amoxicillin prophylaxis. It was several months later when we tried azithromycin and on day 9 her symptoms passed. Over this past year, we've kept her on prophylatic azithromycin. She had many repeat exacerbations when in close contact with GABHS -- in fact we called her our canary because when she starts to ramp, we can take her sister in and she'd be positive for GABHS. We did check her sister for negative cultures 3 weeks after treating to ensure her sister wasn't just a chronic carrier. Exacerbations usually lasted 6 weeks. The issue for us was that she never quite came all the way back and by July this year many of the original symptoms were back. We tried a prednisone burst and this yielded good results for 4 days; however, this was a week after completing the 6 day burst. We did IVIG in August and for the first 2 weeks we were quite worried as things got considerably worse. On week 3, she got substantially better and by now 12 weeks post IVIG she's doing very well. We'll probably keep her on prophylactic antibiotics for quite some time. It is crazy. In our case, she did have the full on body morphology issues and drew people funny. It wasn't a fear of choking thing, it was a straight on fear of gaining weight. Do you think he's depressed? We ended up putting our daughter on SSRIs at an extremely low dose because she had retreated so far into a shell. This was partially because she had no energy from not eating, she also had a pretty severe form of social anxiety, but more than anything else, she was depressed. In our case, it was pretty easy to diagnose as she was making suicidal statements at her doctor's office -- sort of freaked everyone out. Hard to say whether he is just really into computers, needs some escape, is passionate about his work, is hitting puberty or something else is going on. Might be worth raising with your psychiatrist. Regards, Buster

So your history is: pre April -- minor OCD symptoms and chewing of shirt April->July, significant OCD symptoms but upset stomach on Zithromax August -- off zithromax late August -> end of Sept -- back on zith and tried CBT and ERP, no effect end of Sept -> mid October -- tried theraputic dose of Augmentin mid Oct -> now -- using high dose Augmentin (> 800+mg/day) Currently seeing some improvement on high dose Augmentin (rode bike for first time this week), but also seeing some emergence of old symptoms (chewing shirt, tics, etc). What I found most interesting in your post was about Impetigo. A few things that might be relevant: Impetigo is typically caused by either GABHS or staphylococcus aureus. Unfortunately, it is hard to get a good culture of impetigo, but the next time he gets a sore, get it cultured and ask them to check whether it is GABHS or Staph. If it is strep, then ASO is likely meaningless because skin strep does not produce an ASO response. If it is staphylococcus, it's unlikely that oral antibiotics on their own will be sufficient. This would be good to talk with your doctor, but my understanding is that Azithromycin is less useful on staphylococcus. Have you tried mupirocin (Bactroban) on the sore. This is a good topical antibiotic particularly for impetigo. From the symptoms, this sure sound like intense OCD and I can imagine the stress he and you are going through. Yes, I have a child with PANDAS and no I'm not a doctor. Our dd9 had severe OCD symtpoms including requirements about how people went through doorways, ritualistic questioning and culminating in hospitalization when her obsessions prevented her from eating. At this point, I do think the Cunningham tests are likely going to give you the most answers (depite them being a research study). I can see why with the intensity that you are considering IVIG. We ended up going that route as well. Wishing you the best, Buster

Hi Kim, What an interesting thought regarding GlcNAc. There's a very recent John Hopkins study by Dias at http://www.jbc.org/content/284/32/21327.abstract where they found direct correlation between GlcNAc and CamKinaseIV activation. While it is dangerous to connect the three dots, it sure seems like the following is a good working hypothesis: 1) T-cells are producing monoclonal antibodies with epitype GlcNAc 2) The monoclonal antibodies are bonding with GlcNAc and thereby inactivating the ability of GlcNAc to bond with cAMP 3) The lack of available GlcNAc inhibits the suppression of CaM Kinase activations (II and IV) So perhaps what Kirvan and Cunningham are measuring with elevated Cam Kinase II is that the available GlcNAc is abnormally low in the blood serum. It appears that Kirvan and Cunningham are pursuing the direction that the antibodies bind directly to dopamine receptors, but I think the direction you raise in your post is equally interesting and seems to fit the model (i.e., that there's a decline in available GlcNAc). Hmm.... Buster

Hi MomtoCole1: When was last round of exacerbations? What were they, were they severe, are you already on any antibiotics? From what you wrote, the AntiDNAseB, ASO and HHV6 tests would not be considered positive. You can read more about AntiDNAseB and ASO at http://www.latitudes.org/forums/index.php?...amp;#entry25312 Has your child a positive throat culture in last 3 months or other signs of HHV (such as Roseola)? So do you see a significant ramp of symptoms and a remission of symptoms over a 4-6 week period? Has he had significant ramp in symptoms associated with the numerous strep infections? There's debate about whether unchallenged serum is sufficient for testing PREVNAR. It has probably been some time (6+ years) since his last vaccination. I'm not sure what to do with the PREVNAR test. Our immunologist felt it wasn't a useful test in the absence of a challenge (i.e., recent revacination). We have no desire to revacinate. Well, PANDAS doesn't have anything to do with ASO or with AntiDNAse-B values. While some of us on this forum have found the PREVNAR results interesting, we don't have (and neither does the world health organization) good data on what are the typical values in the population 6+ years post vaccination. So those results don't tell you much. Your IgG values look good and at least indicate he's doesn't have something else going on. What are your child's symptoms? How long do they last? regards, Buster

That makes sense to me, but I don't think anyone knows. In the words of Ed Kaplan "despite over 4 decades of intense research, the carrier state remains an enigma." Something keeps the colony in check and seems to disable the M protein (i.e., a penetration factor). They do know that skin strep doesn't cause elevated ASO -- so something in the skin seems to neutralize streptolysin-O . So perhaps the carrier state is really the body has sufficient immune response to stop colony spread/replication, but not enough to clear. Seems like a great experiment to see if carriers have low IgA. I haven't seen any study on that -- but who knows what's out there. Buster

An explanation I used with my Dad was "this is sort of like an allergy to bee stings, as long as she's not stung she's fine... If she is stung then her body produces an antibody that is supposed to go after the bee venom, but seems to interfere with neuronal signalling in the brain too. For reasons we don't understand in some kids it takes a while for the reaction to go down. We think it's because the immune system thinks there is more bee venom out there so keeps making more antibodies." So the chronic part seems to be that the B-cells have the wrong formula for creating an antibody to strep. It appears that neuronal tissue "looks like" the target for the antibody so T-cells keep indicating there's more stuff in the system until the blood-brain barrier closes. Once the BBB closes, it appears that the antibodies dissipate at around 4-6 weeks. If another illness occurs during that time and re-open the BBB again, then the cycle repeats (i.e., you don't need another GABHS infection). Of course no one really knows yet, but this is how I understand it. Regards, Buster

As far as I know yes. Immunoglobulin A (IgA) is found in mucous membranes, particularly those lining the respiratory passages and gastrointestinal tract, as well as in saliva and tears. Immunoglobulin G (IgG) is found in all body fluids and protects against bacterial and viral infections. Immunoglobulin M (IgM), which is found mainly in the blood and lymph fluid, is the first to be made by the body to fight a new infection. Immunoglobulin E (IgE), which is associated mainly with allergic reactions is found in the lungs, skin, and mucous membranes. Immunoglobulin D (IgD), which exists in minute amounts in the blood, is the least understood antibody. Yikes, let me try a simple response and see if this helps: Patients with IgG1 or IgG3 deficiencies are more likely to have chronic and recurrent infections of the lower airways. Patients with IgG2 or IgG4 deficiency are more likely to have sinusitis and otitis. A good reference on this stuff is http://www.primaryimmune.org/publications/...s/book_pats.htm

A carrier is thought to be one who has colonization but no invasion or infection. This means that the strep is on the surface of the mucosal lining or on the skin, but does not get into the blood stream. It isn't perfectly understood why in some folks the strep doesn't seem to get into the blood stream. Some theorize that there is some other bacteria interfering with the colonized GABHS that prevents it from continuing to spread, some believe that the strep doesn't break down the fibrin and hence can't invade without some breach (like a dental procedure). Bottom line, some folks seem to keep a long-standing colony of strep without having any significant invasion or immune response. By the way, this is also why it's hard to clear a strep carrier -- there's essentially not enough blood flow for the antibiotic or immune system to get to the GABHS on the surface of the skin. The skin acts as a great barrier -- this is a good thing. Highly unlikely. It is more likely that the strep just can't penetrate the skin or mucosal lining without help. Yes.

I think this is a great theory and definitely worth pursuing. The high dose of Augmentin would dramatically reduce the ability of the strep that might burst from a cell to replicate and in addition the bacteriacidal nature of Augmentin could actually weaken and destroy those cells at that high concentration. It seems perfectly reasonable to me that our kids already have weakened immune reactions to GABHS and as such don't mount the necessary response to destroy the strep -- either by producing the wrong antibodies or by not producing enough of the right ones. The recommended dosage is for "standard kids who have standard responses" and not for immune compromised kids. So at the high dosage we're either holding the strep in check or actually killing it. I think Swedo has it right that you have a genetic pre-disposition, then the right strain of strep, then the right circumstances that open the BBB. I'd love to know if there are kids with the high rates of the 24.3.1 antibody that don't exhibit symptoms. I keep thinking of the recent mouse model and wonder if the IgG was transferred into normal mice would the symptoms emerge or is it only when the IgG is transferred into similarly immuno-compromised mice. My belief is that we aren't really strengthening the immune system with anything we're doing so far (PEX, IVIG, ...). These are really temporary measures and unless they magically reset the T-regulatory cells we're in this for the long haul (just my opinion). This is why I think we'll have to stay on antibiotics for a long time until some other event resets the immune system (like puberty). regards, Buster

The short answer is likely yes, but it's hard to tell. Part of it depends on what the monoclonal antibodies attach to. In acute rhuematic fever, the antibodies seem to bind to M3 and M18 serotypes of GABHS and the antigen presented is similar to heart muscle. Thus antibodies keep indicating an antigen when it is just normal cells around. In Sydenham Chorea, Kirvan discovered that brain tubulin was a target for antibody 24.3.1. It appears this also applies to PANDAS (although I don't think they have published that yet). So, if the blood brain barrier opens and the blood can interact with tubulin, then I could imagine that the macrophages would report they found such cells and the feedback loop would continue even though no GABHS was found. One inconsistency is that as far as they can find, there doesn't appear to be permanent damage from the bonding to tubulin. This would imply that either the macrophages are not ingesting the tubulin or that the ingestion of tubulin doesn't matter. I don't know enough here to even guess. It does seem, however, that as long as the BBB remains open, there's a strong likelihood of a feedback loop without requiring GABHS antigen. Regards, Buster

Hi Bronxmom2, Do you know which type of PEX you are getting (i.e., one with replacement with Albumin or one with replacement with donor plasma)? I ask, because the one with donor plasma is likely to have antibodies that can take out the strep. If you just have the Albumin then the remaining B-cells will likely find any strep and reproduce the faulty antibody. So, yes, it would sure be nice to be strep free before you go in for PEX particualrly if you are just getting Albumin. PEX with Albumin is usually called PlasmaPheresis. Please remember that antibiotics don't in and of themselves kill strep. They slow it down so your immune system can get the strep. If for some reason your child's immune system can't find the strep, then IVIG is likely the way to go. With that said, I'd still encourage you to check with your doctor on their recommendation. I studied PEX and IVIG and decided that PEX with donor plasma was slightly more invasive than IVIG with a risk of blood product transmission. We don't know a lot about the sterilization of donor plasma, but with IVIG, it seems pretty well scrubbed. In addition, we are hoping that the IVIG does some reset on the T-regs -- this is just hope as there really isn't any study there. PEX without donor plasma (i.e. use of Albumin) probably has good short term benefit. IVIG will probably help take out strep (if there) and might reset the T-reg cells. I just don't know enough about PEX with donor plasma to make a comment. As you say, an agonizing decision, and I don't know how to help here except to say what we did for OCD-primary. Regards, Buster

A brief summary of the immune system Now that we're in a much better space with our dd, I thought I'd post a bit about what I learned regarding the immune system over the past year. Please help me make this accurate with your comments. If any of you know immunology grad students (or are one yourself) please send updates (either through post or IM). Hope this helps... A bit about GABHS GABHS is a bacteria with two cell walls that is encapsulated in a capsule (hyaluronic acid). The capsule is sort of like a stealth enclosure that makes the bacteria difficult for the body to recognize. The bacteria produces a number of toxic substances such as streptolysins, NADase, Hyaluronidase, Streptokinases, Steptodornases, and Streptolysin Pyrogenic exotoxins. When doctors refer to Anti-DNAse B or Anti-Streptolycin, they are refering to antibodies that are created by the body in response to these toxins produced by GABHS. Technically the antibodies are to the toxins and not to the GABHS itself. A bit about Macrophages Macrophages are detectors in the blood stream that find bacteria. There are a series of "sensors" on the cell wall of the macrophage. Probably the most interesting are TLR2 and TLR4 (TLR stands for toll-like receptors). TLR2 and TLR4 "recognize" gram-negative bacteria. When these receptors fire, the Macrophage essentially engulfs the bacteria and then "digest" the bacteria figuring out what were the big features of the bacteria. The macrophages then publish the "big features" on the cell wall of the macrophages and discard the debris of the bacteria. This publishing of the big features is known as antigen presentation. A bit about T-cells/T-helper cells So the macrophage randomly wanders around and eventually bumps into either a T-cell (sometimes called Th0 cell) or a B-cell (known as the memory cells). The Th0 cells looks at the presenting "big feature" and based on a bunch of biasing factors creates either Th1 cells (which go after intracellular stuff) or some Th2 cells (which go after extracellular stuff). The Th1 cells typically turns into more macrophages to go ingest more of the bacteria but can also turn into Killer T cells (that kill off infected cells). There's some other things here, but that's sort of right. Some of the Th2 cells get converted into B-memory cells which produce monoclonal antibodies. A bit about B-cells The B-cells are part of the humoral immune system. If a macrophage runs into a B-cell, the B-cell is able to quickly produce a bunch of monoclonal antibodies that will bond with the antigen injested by the macrophage. These monoclonal antibodies act like "flags" that essentally make it easy for a Macrophage to know which cell to ingest. Essentially a monoclonal antibody bonded to a cell is like a red flag saying "ingest me." Monoclonal antibodies can bond to either the bacteria itself or to the exterior of cells infected by "invaders" indicating that either the bacteria or the surrounding cell should be killed. A bit about T-regulatory cells While the B-cells produce the monoclonal antibodies and the macrophages/dentritic cells find the bacteria and inject them, the T-cells control whether the feedback loop of activating more macrophages gets going. A certain number of T-cells are what is called T-regulatory cells and these cells watch for antigens and macrophages that present "big features" that are the same as a feature of the host. If the "big feature" is the same as the "host's feature" then the T-reg is supposed to suppress production of Th2 cells and slow/stop the feedback loop. It's sort of "yeah, you found one, but that's one of ours, ignore it and get back out there" type of thing. So what does all this have to do with PANDAS Well, in PANDAS it is thought that the antigen (bacteria) bumps into a MacroPhage and gets ingested and the GlcNAc carbohydrate is presented on the exterior of the Macrophage. The Macrophage then runs into a B-cell and the B-cell creates a bunch of anti-bodies for this GlcNAC which go around marking GABHS with the antibody. More Macrophages find these "marked" bacteria and put up a flag saying "there's more GlcNAc around" (this is the antigen presentation). The Macrophages run into a bunch of T-cells and they start creating more Macrophages (and more B-cells to make more antibodies) and the feedback system starts really getting going. The more GlcNAC found, the more the feedback system continues until eventually all the bacteria is ingested and the cycle slows down. What does antibiotics have to do with this? Well, remember that while the T-cells are replicating and the B-cells are producing antibodies, the bacteria itself is replicating. So it is sort of a race to who can replicate faster (the ingestors/killer cells or the bacteria). Antibiotics slow down the speed with which the bacteria can replicate. Macrolides (like azithromycin) prevent the production of an enzyme needed for replication. Penicillin derivatives weaken the cell wall of the bacteria causing many of the bacteria to self destruct. The effect, however, is basically the same, the antibiotics slow the replication of the bacteria so that the B-cells can produce enough antibodies and the T-cells can produce enough macrophages (and killer cells) to take out the marked bacteria. What about intracellular strep? Intracellular strep acts very similar to the ingestion by a Macrophage of a bacteria. Cells have a number of flags they can put on their exterior if they've been infected by a virus or a bacteria. Sometimes the Macrophage can find these cells, but often one has to wait until the cell bursts and then the macrophage has to catch the bacteria before it invades another cell. One theory is that it is this intracellular strep with intermitent bursts that cause the antibodies to stay high because the antigen never truly disappears. I hope the above is somewhat helpful as an explanation... Regards, Buster

We also saw an improvement when adding advil into the mix. We can't say why but ibuprofen was quite effective and we've kept it in the daily regimen. 100mg/day. We've tracked long-term azith usage in cystic fibrosis -- it's about the only studied long-term antibiotic. ARF tend to use penicillin rather than long-term augmentin. We checked with both rheumatologist and immunologist and both were comfortable with dosage with recommendation to consider narrower band antibiotic in the future when other variable are all stable. Regards, Buster Thanks, I think I will bump up the zith. I got so concerned because my pediatrician kept talking about liver function. But I happened to give him ibuprofen last night for a headache and I swear he seemed a little better.

Hi dcmom, We're continuing at 250 mg/day for 60lbs dd and will likely remain at this dose through the strep season. Our reasons are: we're trying to minimize the number of variables we've introduced we saw breakthrough events at 125mg/day pre-IVIG We think that we were actually seeing more the anti-inflammatory and immunomodulating effect of azithromycin pre-IVIG -- so perhaps we were doing more than just preventing infection. Now post-IVIG, her CaM Kinase II activation is substantially reduced (119% versus 253%). We'll look at this again in 6 months and decide whether to lower azith or switch antibiotics. My gut is that you probably want to stay at the 200mg/day. How are her symptoms? Regards, Buster

Wow! That's right up with ours during an exacerbation. What are you currently using for prophylaxis? Is she coming back culture positive? Are you confident that strep is actually out of her system?

Hi dcmom, You are quite right and I fell into the trap of using Plasma Exchange and Plasmapherisis interchangably. Disagree anytime . Anyone know which PEX was used by Swedo in her studies? Was it Albumin or high-mix antibody doner plasma? It is a dilution effect (even with additional donor) since on average, the blood circulates around the body about once a minute (assuming 1 beat/sec). As such, I guess they just keep running the "filter" until the theoretical concentration of host antibodies to new antibodies reaches some threshold. The effect would be the same as having some PEX and some IVIG. Well, we're basically on the prophylaxis until she's 18 or until the research can explain more of what we're seeing (i.e., we're hoping the next decade will figure this out). We will likely return to a more narrow band antibiotic in 6 months or so but really, truly don't want to repeat the past year. What we like about azith is the long half-life. We'd sure be interested in a narrow band penicillin that has a > 3 day half-life. Regards, Buster

Sort of, but not quite. Unlike other auto-immune diseases, the antigens in PANDAS (and in Sydenham Chorea) are not the body itself -- but rather coming from an incorrect response to an external antigen. This means that in PANDAS and SC there isn't the feedback loop that is so debilitating in all other auto-immune diseases. Think of it this way, in PANDAS your body is "allergic" to something that invaded the body (i.e., GABHS). In other auto-immune diseases, your body is "allergic" to itself. Yikes. In PANDAS, your body needs the presenting antigen (i.e., GABHS). Without the antigen, your body shouldn't be making the "naughty" antibodies. This seems to be born out by the Swedo, Kirvan and Cunningham tests and followups at 1 year. This is, however, why the prophylatic antibiotics is so important -- i.e., to keep the amount of antigen (and corresponding antibodies) low. It takes about 4-6 weeks for antibodies to dissipate so hopefully the antibiotics can keep any antibody production way down until they dissipate. This is already a long response to your short question. If helpful, I could start a separate thread on what we know about the immune system and cover this in more detail. Regards, Buster

Yes, PEX depletes and dilutes IgG -- you essentially don't have much of the IgG subclasses at the end and then your body has to make more (typically from bone marrow).

Hi Peglem, I'd recommend against joining the two procedures unless the situation is truly life threatening. I'm not sure how literally to take your question. If you did them at the exact same time, you'd take out all the IVIG you're putting in because the blood circulates around many times and the PEX is logically a dilution action -- i.e., you keep taking out more and more antibodies till you've probably gotten a lot of them. Typically 70% reduction is consider a great PEX response. ** EDIT/correction: dc_mom points out that this procedure is done using a doner plasma instead of albumin. It still has the same "dilution" effect. Apparently plasma exchange is used both for replacing with doner plasma and for replacing with albumin. ** If you meant, "why not do PEX and then immediately do IVIG" -- probably the answer is exhaustion -- you've essentially spent 7+ hours/day over typically 2 days for PEX and have all the complications that might be there and then are doing 7+ hours for 2 days for IVIG. I'd also imagine that the inrush of foreign antibodies in IVIG might have much more severe response if your own immune system isn't up to snuff to take out the foreign antibodies. There are folks who have done this (see http://ard.bmj.com/cgi/content/abstract/61/1/37) but this is typically reserved for life threatening situations where an immediate response is needed and then an attempt to control improper re-emergence of the faulty antibody. Regards, Buster

Hi Bronxmom2, yes our dd9 is doing great now 10 weeks post-IVIG. We had a hard first 2 weeks and then everything settled out in week 4 and it's been great since then -- I can't tell you what a relief this has been and both EAMom and I needed some quiet time to recover. Yes we did. This was by no means an easy choice. PEX had the advantage of what appeared to be immediate results whereas IVIG was looking like 4-6 weeks before we'd see results. Swedo tended to use PEX for tic-primary disorders and IVIG for OCD-primary disorders. Our daughter's symptoms were primarily OCD and the secondary movement disorders seemed more OCD/chorea than a tic. Our biggest concern with IVIG was that we might be introducing some illness that is not yet tested and this haunted me personally and made me want to exhaust the other options before proceeding. The first 2 weeks post IVIG were torturous for I worried we had not only opened the possibility for a blood born illness, but also all her symptoms were coming back. Thank goodness for rock solid EAMom -- it was critically important that we were aligned on what to do so as to be supportive post IVIG. In my opinion, there is no reason to believe that PEX will be more permanent. Perhaps the critical item to consider is that the half-life (also known as the turnover rate) of antibodies is around 4-6 weeks (yes, it varies by antibody, but this is likely close). So, with PEX you'd have to be darn sure that you got rid of the original strep infection otherwise the antibodies will just come back. With IVIG, you actually are likely to get some "correct" antibodies to strep (meaning 1 in the 10000 donors probably have such antibodies) and thus these antibodies actually can take out remaining strep. Second with IVIG, there is some research (Kessel's paper for example) that the inrush of foreign antibodies reset T-reg cells. While this is incredibly preliminary, it gives some rationale as to why IVIG might have longer term sustainable effect over PEX. Now on the downside, we're counting in IVIG on the incoming antibodies (T-regs) recognizing the "faulty antibody" and taking it out. We just don't know how likely this is relative to the very concrete evidence from PEX at removing antibodies. So what you have is that IVIG has a probability of removing faulty antibodies and a possibility of resetting T-regs. PEX has a definite ability to remove the faulty antibodies and is unlikely to reset T-regs. So with all of that and that my dd9's symptoms were more OCD -- we went with IVIG. I totally appreciate why mom_md went with PEX given the severity of their symptoms and the higher tic component. Both approaches seemed effective. No matter what it is incredibly stressful to decide on either course. Actually, it isn't the T-cells, but rather the T-regulatory cells. It may also be related to B-regulatory cells. We're pretty certain T-reg cells are involved because the antibody is targeting GlcNAc carbohydrate which is a host carbohydrate. T-regs would normally suppress this antibody, but for some reason aren't. There is research that high levels of dopamine seem to suppress T-regs -- so perhaps that is the connection. We don't know. Regards, Buster

Hi Bronxmom2, The post by ShaesMom is quite good. With PANDAS, it is thought that there are three things going on: 1) The production of an anti-host antibody in response to a sentinal GABHS infection 2) A failure of T regulatory cells to control the replication of the faulty antibody 3) A breach of the blood brain barrier that allows the faulty antibody in the blood to reach neuronal tissue Short term prednisone has an effect on #3 (i.e., lowers inflammation) and can also have an effect on #2 (by suppressing immune response similar to what T regulatory cells are supposed to do). It is unclear if prednisone affects #1. Plasma Exchange (PEX) directly remove antibodies (i.e., affect #1) and can have an anti-inflammatory effect (i.e., #3) if the cause of the inflammation is antibody related. IVIG has significant anti-inflammatory effect (i.e. affects #3) and also affects T-regulatory cells (i.e., #2) (see Kessel's paper http://www.jimmunol.org/cgi/reprint/179/8/5571 ). It is possible for IVIG to affect #1 (i.e., anti-host antibody production) as well by either providing the correct antibody to take out an antigen (hence reducing bad antibodies) or by overwhelming the immune system with foreign stuff such that the T and B-cells don't produce so many anti-bodies. In any case, the effect of IVIG is thought to be primarily #2 and #3. Regards, Buster