eljomom

HOnestly, if you are going to go to an LLMD anyway, at least let them order any tests they would specifically be looking at....I am truly not saying this based on anything other than the fact that many of us, who did throw down a chunk of change (not $1200 but a few hundred anyway) are still questioning the results we got, even though they say "negative". I don't know, really. Just throwing it out there. Question---you said chronic staph---can I ask how you tested for that??? Three of my 4 kids passed around Impetigo (only cultured my son--it was staph) for 3 months this summer. My PITAND kid went crazy with the tics shortly after a high fever, and very, very shortly after had a major skin infection that I didn't know at the time was Impetigo. It wasn't till my son got it bad that I treated him--go figure. Saving my baby from "unnecessary antibiotics"---huh....anyhow, I wonder why it was so hard to eradicate in this house....You can PM me if you'd like.

oops, duh...just read the rest of the title to your post....guess you are saying the other 55% IS pitand?

maybe the other 55% is PITAND??? like us:) funny, I was going to call her too...now i don't have to...

Yes! in Northern VA

Tests lyme specific for "cytokines" and T cell, etc......all the lovely things implicated in PANDAS. Wonder if there's a test specific for these things for pandas? well, strep, staph, etc....

Was the c. diff from prolonged abx? My daughter did 3 rounds of flagyl, and finally vanco. was the kicker with Culturelle....

What is the Immunoblot? That sound more accurate...

My oldest had "c. difficile" when she was 2 (not my pandas kid).....don't know if its the dame as clostridia, but she had mucousy, stools with blood up to 20 times a day. Horrible cramping every time she ate. My ped. was not interested---just give her fluids. IT wasn't until my neighbor (an RN) was at my house when I was changing a pullup and got wind of the SMELL!!! It is DISTINCT. Period. NOT like manure to me. Manure would be delightful in comparison.

I think--possibly---that vancomycin is "the mother of all abx"??? My oldest dd had c-diff when she was 2 and went 3 rounds of flagyl. every time she would go off, within a week, c diff would be back. Vancomycin was the cure, along with major probiotics. Echolalia is something in the Tourette's/tic family.

Was just re-reading this, and what I really, really would like understand is how that can be a valid, realistic statement?? That "only one of these is needed to confirm evidence of exposure to Bb and can confirm a clinical diagnosis of Lyme disease." My dd was 31+, which ended up being negative after confirmation test----and Dr. Harris said it was because 30-31 are cross-reactive. So how can it be said that 30 and 31 are "known Bb specific"???? Also, if you read Dr. Crist's Lyme made easy, he says that "exposure to Bb" does not mean "active Lyme" infection. This is where I think sometimes people are being treated from "exposure" (thus antibodies are present) but not active disease. Sort of like taking abx thinking it would make the titers come down. If the infection is cleared---which can be proven--but titers are still high, it's just cuz they are still high. Does that make sense? Not trying to ruffle feathers---really just trying to understand before I take my dd into the Lyme plunge.

Buster---PM'd you..

If you do any research on IVIG, and I've only done a tad...but I read over and over how the speed at which it is given affects the side effects, and it's very important to be careful with that.

fr88---that is my biggest fear---making things worse. I too am surprised to see that Vit. D and NAC made things worse. I give dd Vit. d daily, and was thinking about trying NAC. How did you figure out those things specifically? Also, were you IgE allergic, or did you have IgG/IgA sensitivities? Foods? VERY interesting about the Th 17---check out the post I made earlier with a link--I think it was the one where they were speaking of this exact thing! On second thought, that might not have been the link I posted??? but I just read this today and made a note to check into this Th17.

Sorry for even more questions, but it also sounds like your IVIG was not successful? YOu mentioned that you had major problems from it.....can you elaborate? Sorry again to press, but this is my fear for my 7 year old---is it worth pressing the IVIG? Thanks so much for your openness with your personal information. Also, I just want to add, that sometimes many of us might react/respond in a way..or even present things in a way...that comes off more intense, defensive, accusative, etc. than intended. We are all a bunch of "mamma bears" here, (and a few pappa) who are desperate for the health and well-being of our children. Thanks for coming back--I think we have only gain from having a seasoned Pandas-survivor here.

How do we find "neutral"--I really would like to see someone like this. NOt someone who kicks you out the door if you are not "CDC psoitive" but not someone who makes everything Lyme....anyone? beuler? This is EXACTLY what I was told 3 years ago with my positive IGM and negative IGG. 3 years later, and, after 2 years of intensive antibiotic treatment (including IV), I continue to test IGM positive and IGG negative. It has FINALLY been determined I never had Lyme and will most like test positive IGM forever. Just something cross-reacting. (they suspect EBV) It happens a lot with IGM. I was positive even by CDC standards.....with all 3 "specific" Lyme bands positive. Just letting people be aware there IS another side to this. Please be careful. Thanks Pmom! I appreciate your side as well! All I can say, is after 22 months since this last episode began, I am finally seeing real results. But honestly, I do like hearing all opinions. So what do you make of my daughter's positive Quest RMSF? (I'm asking this in true honesty...not sarcasm) --Thanks- Melinda Melinda, I have no experience with RMSF, so, I can't give you any answers. From what I read, though, most people become hospitalized from RMSF......was there a time when your child was severly ill? (not talking tics or ocd...I mean severely ill that she had to be hospitalized?) Anyway, I don't know if it is possible to have RMSF and never know it....perhaps.....like I said...don't know much about it. But, given the inaccuracies of tests these days...I would probably get a second opinion, maybe even a third, on the RMSF thing......and I would go to someone neutral who doesn't see tick borne disease automatically. And I am glad your daughter is doing better.....regardless!

Not even sure what rabbit-trail I was following when I hit this---something about bbb... "Also, ask your practitioner about the supplements I have created specifically for blood-brain barrier integrity, brain inflammation and increased blood flow to the brain (which will be discussed in my next book). " My link

I have to disagree here---IGENEX does NOT ONLY test for Lyme specific bands. As you state, "CDC wrongfully includes five non-specific cross-reacting antibodies in its Western Blot criteria:"---all of which Igenex tests for!! And quite honestly, what has sparked my interest in this is that there are many PANDAS kids who's Igenex results have been posted (including mine) -- many of which have positives for 41, 58 and 66. What would be really helpful it to know what those 3 bands cross-react with...and bingo, maybe we'd have an avenue to pursue for the pandas!

Now the greatest outcome of this venn diagram would be to then try to use it to figure out which treatments worked best for which subsets, etc...... ie., if you have ocd AND SC--"x" was most helpful if you had tics only "Y' was most helpful if you had NOT sudden onset.....you know, it could go on and on, but in the end, this is what wee are looking for. I don't really give a rats **@*# what it ends up being called, because it's NOT one-size-fits-all here---but how do we help the symptoms we each do have. Buster, I think this is a great tool to get that started!

smartyjones---other than strep, myco p and lyme, what did you have tested?

I just read something last night that was talking about how they have not "tested" for carditis, etc. in some of the defined pandas or SC kids---or something like that. I just remembered when I read it thinking---oh, then left that stone unturned---maybe I should be checking my daughter for carditis too! Also, episodic tics would rule me out of pandas/pitand alltogether, because once her sudden explosion of tics, they have not been "episodic" whatsoever. Morphing from one thing to another, so maybe it was a month of jaw thrusting, head nodding, head shaking, finger flicking and sniffing, eye widening, blinking, etc .... that turns into mouth stretching/tongue thrust and curl, snapping head back, intense eye blinking, etc...so in our case "episodic" I still believe does not fit. She does have CamK 168, and high anit-lyso and anti D1 too. Hmmmm.....anyone else's tics not "episodic"? Sorry, I don't mean to take this thread on a rabbit trail

OK Buster---I think I"m getting closer to the a-ha moment! You are really clarifying many things for me. So, let me make sure I am uderstanding if you don't mind: it seems there are really 2 more distinct types of pandas/pitand kids here---1 type that responds to antibiotics because it shuts down the bacteria, and the antibodies eventually die out, and the exacerbation resides. Then there is the second kid (mine) who continues to have symptoms even after the bacteria/virus is gone because now the antibodies are going after self-tissue (in the basal ganglia)....and at this point, antibiotics are not going to be as helpful (other than the POSSIBILITY of them helping with inflammation,etc...)??? If so, this should guide the course of treatment, right? Also, the Cam K being high in "normal kids" with active strep might be saying that Cam K scores are more relevant to Kid #1 described above, and once infection clears, and antibodies die off, all is good in the world. And that anti-neuronals might then be a better tool for the kids who continue to have symptoms beyond the normal "antibiotic clears illness---antibodies die off" because these auto-antibodies indicate that there is truly AUTO-IMMUNE (hence ANTI-DOPAMINE, etc.. ANTIBODIES) problem going on??? So the million dollar question then is: What do do if your kid falls into #2?? You mentioned steroids helping if the problem is outside the BBB, but if it's across the BBB---do steroids help close it? Or do you go straight to IVIG---does that help close it? And the 2 million dollar question is: do you take these extreme measures if your kid is still functioning? Ticcing like CRAZY, ocd is not non-functional, hyper, sep. anxiety are tolerable b/c we homeschool....what then. It's so hard to do nothing when you know what is likely happening. Why wait for it to get horrible, and why not do something if you can? Which leads me to the 3 million dollar question---does IVIG really work and "cure"? And I really haven't looked into the possible negative-impacts of these things yet, but is it worth risking those things and making things even worse....these are the decisions I lie awake at night pondering.... It sure looks like at least 24.3.1 is causing Cam Kinase II activation. There may be a couple other antibodies that are doing it too, but 24.3.1 seemed to be both an anti-lysoganglioside (discussed in a moment) and a CaM Kinase II activator. Yikes. Well, let me try an explanation here and we'll see if it help. CaM Kinase II activation is generally tested by assay or microplate. A sample of blood serum (which contains antibodies) is incubated with neuronal tissues (typically those from neuroblastoma cells) to generate a potential CaM Kinase II sample. The sample is then incubated with a microplate substrate in the presence of a radioactively tagged ATP. Consider this a radioactive flag that signals that a particular type of activation is occuring. There's a bunch of steps next that wash the substrate, but the end result is that the microplate will have a radio-signature that indicates a quantity of CaM Kinase II activation. While in the Nature paper, Kirvan isolated and cloned the 24.3.1 antibody. These days I think they test without isolating the individual antibody, but rather taking a diluted sample of blood serum and seeing if any of the ATP changes state (i.. raises the flag). If it does then they assume the likely cause is the 24.3.1 antibody. It's a pretty good bet. Now CaM Kinase II regulates Calcium channels and potentiation (meaning keeping channels open). This has effect on cell signalling (particularly fo neurons). So lots of CaM Kinase II activation likely means a lot of neurons would be firing. It appears it is elevated from a specific antibody (which is an autoimmune response). Absolutely. Here's the way to think about it. When you get an infection, your body produces antibodies to help find bacteria and flag it. Quite literally antibodies are little Y shaped structures that attach to specific carbohydrates or proteins on a cell surface. They flag for destruction. There's these other cells known as macrophages that come along and see the flag and "eat" the bacteria. The macrophages then send a signal saying "found some" or "make more antibodies" (this is a short hand, there's a lot going on here). Anyway, the body makes more antibodies and more macrophages until the infection is resolved. Now when the infection is gone, the anti-bodies will still be around for a while (typically 21-28 days). This is actually a half-life. This means every 21 days about half the antibodies have been used up. Now this assumes you don't get another infection that ramps everything back up. In auto-immune diseases, a portion of the host can act as a recipient of the Y antibody. This is a mistake (i.e., the immune system is supposed to not make antibodies that will bind with host cells. For whatever reason the check of "is it going to attack the host" is broken or ineffective so the feedback cycle starts. The target of the auto-immune disease (think neuron cells) now acts as if it were the bacteria. The immune system sees these monoclonal antibodies and tries to engulf the cell. Do we know that this is what is really going on.... not really, but it sure seems plausible. You could therefore ask how do you break the cycle? Well if the stuff is across the blood brain barrier, closing the BBB helps break the cycle. If the stuff is heart muscle or joints or ... then prednisone can help break an autoimmne cycle. It is not known whether the antibiotics are having an immunomodulating effect, an antiinflammatory effect and closing the BBB, or some other effect. Please post again if above isn't clear. Buster

Also, forgot to add, but I had a hard time with the ocd scale, as I really don't know how much the thoughts of germs are in her head. It's so insiduous to me....she will not eat anything that has been touched, won't turn her head my direction if I pick her up (my breath), etc....so many things I didn't realize b/c she doesn't verbalize them. The not eating from germs was obcvious---"you touched it!!!"....but the time she mentioned that she flicks her fingers (a tic in my opinion) to flick the germs off---that one is tough for me to rate.

Meg's Mom---I did the scale for tics for my daughter, and she went from an 8-9 to a 28-29 within a two week period following the high fever. But my problem here is that she has stayed elevated like that for 6 months now. I do believe still that there is definitely an autoimmune issue, and that even when the bacteria/virus is cleared, the autoimmune issue has not been shut down. Does that make any sense?? iceberg tip = speaking to the choir on that! I cannot stand the terms wax & wane. Hate them with a passion. Those 2 little words kept my child in a *&*% place. Here is the deal. If your child is a 15 on the Y-boc score, and sometimes goes down to a 12, and other times is an 17 - that is wax & wane - could be an autoimmune contributor - more confusing. If your child is a 15 on the y-boc score, and then goes to a 28 - then you likely have somthing else going on, and you need to look at PANDAS. It's an exacerbation. If your child is an 8 on the y-boc scale and goes to a 28 - then you definitely have an issue - something like PANDAS - IMHO. There is really no reason that you can't have a tendency to OCD & then get PANDAS on top of it. That is a very bad situation.

I have to say that I am still a bit confused about all this. So what I'm hearing from fr88 is that the anti-neuronals are ONLY elevated from strep antibodies? and that the Cam K really is totally (possibly) unrelated to strep? It sounds like the antineuronal antibodies, then, are really the only indicator on Cunningham's test that it is "PANDAS"---strep-related, and that Cam K means what? Maybe auto-immune, maybe not? Sorry for all the questions---just really, really want to understand this. My daughter had no strep titers---may have a year or so ago, but wasn't taking her in for sick visits at that point, as my first three were on so many antibiotics they developed allergies to them....so, she is PITAND. Anyhow, her CamK was 168, and anti D 1 was 4000. I still don't hear definitive based on those things that it means pandas/pitand and not tourettes/ocd.

Wow Buster---your explanation is what I have been looking for! Thank you for taking the time to put all that out there. I have actually been thinking about calling Swedo, but doubt she would talk "off the cuff" and give me the real deal. So this antibody 24.3.1---is that what the Cam K is responding to? Can you explain how they are testing that specifically? Sorry---I'm a "need to understand" person...and I am lying awake at night trying to figure this all out. I keep thinking I understand the Cam K, but then I realize I really don't. Is it elevated from inflammation, from the antibody, or from an autoimmune response? Since my daughters symptoms started suddenly, and have not remitted, then does that mean the "cause" is still lurking (which in my heart I truly, truly doubt), or that the autoimmune process was set off, and is still causing symptoms? Can an autoimmune illness cause symptoms even when there are no bateria/viruses going on? This is what I don't get.... Thanks again for your patient responses, Buster. Hi Eljomom, I absolutely get your question. The reason all the studies were on strep is that Swedo was looking at sudden onset OCD in kids who developed sydenham chorea. Sydenham Chorea is generally accepted as a sequela to untreated GABHS infection. She noticed that sometimes the OCD came before the chorea and sometimes after. She then got some kids with sudden onset OCD but didn't get chorea. That's weird (she thought). Is the sudden onset OCD something else? About 21% of patients who get Acute Rheumatic Fever gets sudden onset OCD. About 30% of patients with Acute Rheumatic Fever get Sydenham Chorea, but only 70% of those who get SC get OCD and apparently a few kids (i.e., the 50 she was looking at) get OCD but no SC. So now she's thinking -- I wonder if the SC and OCD are triggered by the same antibody or is it two different antibodies. She found in a really small study that two kids with sudden OCD but no SC had strep and another two kids with sudden OC but no SC had a virus. So now she's stuck. It could be that it's caused by strep or caused by a virus. She tried immunomodulating therapy and all the kids got better. Now that's weird (she thought again). Others tried treating the OCD in SC kids with IVIG and they got better too. Wow! Another group tried treating OCD in non-SC kids and they didn't get better at all. Hmmm, somethings going on here. Maybe this sudden onset is the thing. She's got a bunch of people around her who know tons about streptococcus so she focuses there first. Here's the key -- it's possible sydenham chorea might also be streptococcus and viruses too... Everyone sort of thinks it only comes from untreated strep -- but maybe not. So the team starts looking at just untreated streptococcus -- she thought this would be easy to prove, then they could come back to those pesky viruses. But now here's the key problem she ran into.... In her original definition, she said that PANDAS was sudden and dramatic onset of OCD and/or tics. Kurlan flipped out and said "all tics are dramatic and sudden". So Swedo's stuck -- how does she look for these auto-antibodies if she doesn't have a good way to separate out the kids who have them from the kids who don't. Swedo landed on these comorbid or coincident psychological manifestations. The kids who seeemed to fit this PANDAS profile had separation anxiety and daytime urinary frequency and other such symptoms. So Kirvan and Cunninham used serum from a group of kids who had OCD and these other symptoms and started looking for the preverbial needle in haystack and found antibody 24.3.1. Now the question is whether the kids with just tics caused by auto-immune have this 24.3.1. We frankly don't know. Kurlan sort of refused to pursue any kids with the dramatic onset of OCD (i.e., he stuck to kids with long term tics) and kept not finding the anti-basal ganglia antibodies. Most likely because he didn't actually have any kids who fit the expanded PANDAS profile (i.e., the ones with seperation anxiety or daytime urinary frequency or dilated pupils, ...). So I totally get what you are saying that "what happened to all the folks who are affected primarily by non-strep" -- right now Swedo still doesn't have everyone agreeing that 24.3.1 (cunningham's tests) are meaningful. So she's still working that one and until she can prove that, there's not a lot of money/research being spent on other harder to find viruses and bacteria. Buster