norcalmom

here is someone at Brown university, about 45 minutes from Boston, that wrote a paper with Swedo in 2004. There is a researcher at Brown, not the one on this paper, that did a bunch of work early on, and I've heard Swedo cite her (recently at the texas symposium a couple weeka go) and in papers too. Maybe an email to the person below (email is on the abstract at the bottom, if she still uses that address). Good luck. Henrietta L. Leonard a1 c1 and Susan E. Swedo a2 a1 Department of Psychiatry, Brown University, Providence, RI 02903 USA a2 Pediatric and Developmental Neuropsychiatry Branch, NIMH, Bethesda, MD USA Abstract The evidence to date, both published and unpublished, which addresses the validity of the proposed unique subgroup of children with early and abrupt onset of obsessive–compulsive disorder (OCD) and/or tic disorders subsequent to streptococcal infections was reviewed. The aetiology of OCD and tic disorders is unknown, although it appears that both disorders may arise from a variety of genetic and environmental factors. Post-streptococcal autoimmunity has been postulated as one possible mechanism for some. The acronym PANDAS (for paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) has been given to a subgroup of paediatric patients who meet five inclusionary criteria: presence of OCD and/or tic disorder, pre-pubertal symptom onset, sudden onset or episodic course of symptoms, temporal association between streptococcal infections and neuropsychiatric symptom exacerbations, and associated neurological abnormalities. The proposed model of pathophysiology provides for several unique treatment strategies, including the use of antibiotic prophylaxis to prevent streptococcal-triggered exacerbations, and the use of immunomodulatory interventions (such as intravenous immunoglobulin or therapeutic plasma exchange) in the treatment severe neuropsychiatric symptoms. For the latter study group, long-term (2–5 yr) follow-up revealed continued symptom improvement for the majority of patients, particularly when antibiotic prophylaxis had been effective in preventing recurrent streptococcal infections. In addition, the episodic nature of the subgroup's illness provides for opportunities to study brain structure and function during health and disease, as well as allowing for investigations of the aetiologic role of anti-neuronal antibodies and neuroimmune dysfunction in both OCD and tic disorders. Although much research remains to be done, an increasing body of evidence provides support for the postulate that OCD and tic disorders may arise from post-streptococcal autoimmunity. The unique clinical characteristics of the PANDAS subgroup, the presence of volumetric changes in the basal ganglia, and the dramatic response to immunomodulatory treatments, suggest that symptoms arise from a combination of local, regional and systemic dysfunction. Ongoing research is directed at understanding the nature of the abnormal immune response, as well as identifying at-risk children, in order to provide for novel strategies of prevention and treatment. (Received September 11 2000) (Reviewed December 13 2000) (Revised February 25 2001) (Accepted February 26 2001) Key Words: Obsessive–compulsive disorder; tic disorders; Tourette syndrome; streptococcal infection; basal ganglia disease. Correspondence: c1 Address for correspondence: Dr H. L. Leonard, Child Psychiatry, Rhode Island Hospital, 593 Eddy St., Providence, RI 02903, USA. Tel.: 401-444-3762 Fax: 401-444-8879 E-mail: Henrietta_Leonard@Brown.edu

WE don't have any issue with it - but my DS tested slightly low (just like 90% of the population apparently) before I started to give to him. I was tested to in a yearly physical exam -seems the docs are regularly testing everyone for this - and I was also low. We do drops on occasion - probably 3/4 times a week, I'm trying to do more now that cold/flu season is here. I've never noticed any side effects. I put two in his cereal when I think of it (kind of like Vit D roulette - did he eat that bite of cereal/mild where it landed?!). If you child has issues with it, perhaps he/she has gut or liver issues or some inability to process it OR fats (it is fat soluble, and needs suffient fat to work), or maybe they already have enough? Also interesting that LLM's son the same with Vit D and fishoil - I know at least codliver oil was used as Vit D supplement, and I think I've read that reason most northern Europeans (and all northers like Eskimos and Canadians, Russians) who don't have much sunlight, usually have a diet very high in fatty fish - thats were they're getting the Vit D in lieu of sunlight. Here is a god summary I can across: http://ods.od.nih.gov/factsheets/vitamind

I dont' know why this is common with pandas kids - but I've seen it on the board before, and my DS had it as well. He had it before and during antibiotics. And not just at night - he was very sweaty during the "beginning" (more accute) phase. He's not now, but I'd say it was several months.

I just started giving sone NAC last week. Only 700mg per day, so very low dose. He's 120lbs. I think I've seen some mood improvement - he's been happier and chattier. Is it possible for for low does to have reaction that fast, or is it the placebo effect (happening perhaps to the GIVER of the meds!)? Can it effect sleep does anyone know?

never mind - I got it!

Hot? as in fever? I'd try a couple advil for a day or two .

I don't think any one knows for sure. In sitting with the scientists from Cunningham's lab in Texas at dinner, one mentioned that this area of study was less interesting for him if it is"only a signaling problem" (which it appears it MAY be) because it's is a less compelling area than something that actually damages your brain - like MS (another autoimmune disease - which does actual damage the brain permanently. ) And, when I look at the numbers - most kids don't go all the way back to 100% in the studies. We all can, and should, try to get our kids there - but after the infection is gone, and the Auto-antibodies have been removed, CBT has been used...some of kids still have symptoms, and/or they catch some thing that makes them re - exacerbate. (because the genetics, or the immune issue or whatever it is, is still there in your child) I hope for 100% remission. Cured? Maybe as adults - but no one knows that either! (Swedo told me her original 50 pandas patients were fine as adults - but her anecdotal info isn't an actually survey, and her idea of "fine" or "better" and my idea of 100% are most likely different! In SC, I have read a study that a percentage of adults still had some OCD, that began with the SC, and that is what pandas is based upon, but these kids don't usually get intervention beyond antibiotics and sometimes phych meds. But the good new is that SOME kids do go back to 100%, and MOST are able to get back sub-clinical symptoms, and that CBT works as well. And, we don't know what percent will end up with refractory OCD, maybe none of them will.

I don't think anybody does great with a huge amount of candy. I didn't listen to the whole video - just the beginning. My child doe not have big reactions to sugar either, not any different than other kids as far as I can tell. Also, if a kids had yeast issues - (mine doesn't so I wouldn't know this) - would an over abundance of sugar just feed the yeast - couldn't that be the issue not pandas? I do think that an aniinflamatory diet can help our kids a little. We went gluten free for one month, and saw perhaps a little difference, but certainly he wasn't clear correlation. Also, if a kids had yeast issues - (mine doesn't so I wouldn't know this) - would an over abundance of sugar just feed the yeast - couldn't that be the issue not pandas? My experience with the gluten free thing just made me more aware of the carbs in my family's diet. Helped me balance things. I think that the gluten free thing is somewhat anti-inflamatory, just like augmenting with fishoil, tumeric, etc. But it might depend upon what you replace the gluten with as well.

Pay her for her candy. We let our kids go alittle nuts for a couple days - they when they are sick of it - we give them $ for the stash! Like 25 cents a peice for good stuff etc. I'm also planning on giving DX some advil for a couple days. The other thing is to introduce "the Sugar challenge" right after halloween - we've done this withboth kids before - for 30 days they have to read labels and not eat any sugar, reward at the end. They learn alot about what has sugar in it and what sugar is called on labels if nothing else!

IVIG and Pex - you can read that study. This is the original data from 20 years ago. yes - their work is all about infections that have resolved. The autoimmune conditions that exist after they are gone. So yes, that is exactly what is going on. That is why they don't feel comfortable saying all kids should have antibiotics long term. They need to study that. Many parents report that kids just do better on antibiotics for some reasonl. They aren't sure why. They theorize it goes beyond the actual active infection and may have more to do with other properties that antibiotics have - some are antiinflamatory, or immune modulating in some ways that isn't clearly understood. Swedo's original study focused on tics, and now seems she is try to distance pandas from tics due to controversy with tourettes people, and tics in general. You can't define tics as overnight onset or not, because they are always abrupt. She does list them as a comorbid symptom - "motor abnormality" I don't know if RF can become chronic. It is likely to come back if antibiotics are not used first 3-5 years after diagnosis according to this site:http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004388/http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004388/

OK - here are my notes. Don't quote me on any of it - these people are presenting their life's work in 45 minutes or less, and I understand only a little of what was even said! Symposium notes day 1 A number of speakers from different disciplines of post infectious immunity presented their area of specialty or research. The point of this day seemed to be to connect pandas researchers and doctors, make them aware of each others areas and current thoughts and research. What I heard mentioned in every presentation at some point (be it MS, Lyme, Cardiac…) was that patients that had early, aggressive treatment faired much better than those that waited. Examples from 3 different presenters (somewhere in their hour long presos) MS – one very aggressive study recently done showed that if bone marrow replacement done in very early stage of disease – there were NO flairs for 36 months after in any patients (only 4 in study). This is consistent with other MS data that was shown (although number who flared and how often, less remarkable). For those that were further along in the disease, no improvement resulted with BMT. Lyme – Again, if caught early and treated with appropriate antibiotics (which is not a 10 day course – it’s a longer, heavier course), a very, very high chance of complete recovery. The longer the disease goes unchecked – the lower the chances of 100 percent recovery, and the more intervention required to effect recovery (IV antibiotics.) And- Autoimmune Myocarditits – if caught early curable, if not caught can become chronic and lead to dilated cardiomyopathy (sometimes fatal). Noel Rose talked about the how the Progression from viral infection to autoimmune heart disease is cytokine-regulated. And his work finds that Interferon-gamma (IFNγ) is protective in myocarditis And IL17 production is increased in the hearts of –/– IIFNγ mice with EAM Also – • IL23, but not IL12, is required for the development of myocarditis • Th17 cells induce severe myocarditis, compared to Th1 cells (those lead to less severe form) He also has some mice studies showing that mice with Th17 can be protected from developing Dialated Cardiac Myopathy by vaccinating with IL-17 antibodies (they gave the mice the antibodies after the infection / automimmune process started, they still got sit, but not the deadly from of the disease) Don’t quote me on any of this stuff. Day one was way over my head. I watched a few you-tube videos on immunology by khan academy (fabulous by the way) in the airport on the way to the symposium, and that is the extent of my background in immunology! At least I got the gist of what the day one presenters were saying. It became clearer as the day went on how complex post infectious immune disorders are. Many factors are being dealt with. Most presenters said that they thought genetics, environment, viral/bacterial infection, something effecting BBB and timing of exposures all played a role. Very complex. Almost infinite number of possible combinations and permutations to explore…and the last presenter was a woman studying genetic analysis – all she does all day is crunch numbers for GWAS, genome wide association study – to provide unbiased genetic complex etiologies of neurobehavioral disorders. She is looking at schizophrenia and Autism at the moment. dinner – I sat with some postgraduate students from Cunningham’s lab during dinner. What was interesting was that these young scientists are so disconnected from what they are actually studying. I think I’m one of, if not the first pandas parent they talked to. One confessed that he was doubtful the conditions existed until Cunningham played a video of a girl with severe Chorea (not pandas patient – SC patient). I think Dr C was good to bring almost her whole team out there to expose them to some of the real world beyond the lab, especially the newer members. Anytime we have the opportunity we need to thank them and point our how they changed our lives, and the course of our children’s lives, and how important what they do is we should do it. (and these are people that benefit from Seeing proof -they are after all research scientists! ). Day 2- Day 2 was mainly pandas presenters day. Unfortunately we lost many of the doctors that were present on day one. We did gain parents however, three of whom presented. They all had very moving stories and made the disorder not just personal, but real to those that only look at mice or cells day in day out. Swedo- She is keeping the study criteria Very, very tight I hear. She wants kids after the first, or most, second exacerbation. It’s a barrier to participation because - IVIG is scary, and so is a lumbar puncture, two MRI’s and many blood tests and traveling with a pandas kid in first exacerbation (?!), so most want to try antibiotics first (sound familiar???!! Didn’t we all?!) and if you do that – you will be ruled out of the study. I heard there are less than 10 in it so far. I asked if a significant number of those kids also have Lyme – she said no, but she thought that most of the kids are from low-risk Lyme geographies. She is currently writing study for Lyme (I’m assuming presents like pandas). She said the pandas study going very well right now.(except in terms of participants – that’s from someone else not her). The A in PANS stands for Acute-onset. Not Autoimmune. I commented that the “overnight onset” wasn’t always “overnight” – and told her how my son presented, and the problem with the word. She agrees – said his presentation not uncommon, and even mentioned Murphy’s “mini exacerbation” theory (one of the reasons I don’t see my child as “overnight” – its something he did a couple years ago, but at a much milder level. I think she is keeping the focus on overnight onset and strep because she has to keep it really tight just to get numbers and acceptance she needs for the med community to believe it. Here is DRAFT criteria for PANS dx. Note that it does not include Strep – pandas is a subset of PANS. I think this was also in “a way forward”..I know I’ve see it before. DRAFT Criteria for Pediatric Acute-onset Neuropsychiatric Syndrome (PANS) I. Abrupt, dramatic onset or recurrence of obsessive-compulsive disorder (Eating disorders may be an alternate manifestation of OCD and are counted here) II. Concurrent presence of additional neuropsychiatric symptoms, with similarly acute onset, from at least two of the following seven categories (see text for full description): 1. Anxiety 2. Sensory or motor abnormalities 3. Behavioral (developmental) regression 4. Deterioration in school performance 5. Emotional lability and/or depression 6. Urinary symptoms 7. Sleep disturbances III. Symptoms are not better explained by a known neurologic or medical disorder, such as Sydenham chorea, systemic lupus erythematosus, Tourette disorder or others. Note: The diagnostic work-up for PANS must be comprehensive enough to rule out these and other relevant disorders. The nature of the co-occurring symptoms will dictate the necessary assessments, which may include MRI scan, lumbar puncture, electroencephalogram or other diagnostic tests. She also had a slide that show how she sees this break down: PANS is a Very large group – PANS Subgroup 1) PITANDS – infectious triggers (has two subgroups a, and a)Strep (pandas) b)Other microbes – Lyme, mycoplasma, others? Subgroup 2) Non-infectous triggers a)Environmental, metabolic, others?( Vaccines Impact of Reye syndrome and Aspirin -ban?) Cunningham’s Cunningham: Presented her usual stuff from the auto-antibody SC v pandas vs. normal and Cam K II numbers. New was the fact that she is correlating certain antibodies and D1 or D2 to symptoms. I don’t have the numbers (sorry! – anybody catch them?) it was something like high anti- Lyso usually present with tics. And Hi D2 with anxiety (and pandas in general) I think they want to focus on the D2 because they can develop drug therapies to regulate this. (this is my theory, not what was said). She said they are trying to get he lab off the ground – and they even had a slide with a name on it…something like Molecuary Labs. I asked her about raised Cam K in non-pandas recent strep kids, because she has said that the median for that is 135, and she said that the range doesn’t really go above 139 or so for those kids. Thienneman: Psychiatrist. Talked about barriers to diagnosing pandas. Even Swedo said “there are about 10 good pandas doctors in the US” . Theinneman also talked a bit about CBT in conjunction (if necessary ) a low does of SSRI (or other) when kids are ready for it being most helpful. She borrowed a graph from a marketing book called “Crossing the Chasm” on Early Adopters. The same mentality is needed to cross the chasm in the medical community. If you read that book, or “the Tipping Point” both are similar – and the medical community is no different. It takes time, and spin and a certain amount of serendipity for a disease or disorder to get recognized and treated on a wide scale. Any doctors we are currently dealing with are “Early Adopters”. At least from the standpoint of seeing the possibility that things aren’t what you thought. She talked about the evolution of accepting disorders of the mind as diseases of the body/brain. What’s scary is just how recently this change has occurred. Theinneman also talked a bit about CBT in conjunction (if necessary ) a low does of SSRI (or other) when kids are ready for it being most helpful. Thienneman used to be an internist. One of the barriers to diagnosing something that doesn’t fit the mold, or even considering a different mold, is just BEING a pediatrician. They have 10-15 minutes per patient allotted on usual days. I loved her line “Hey, the biggest reason I switched from internal medicine to psychiatry is - I get an hour!” “and even that sometimes isn’t enough”. She had some graphs of her pandas patients and symptoms before and after interventions – interventions include IVIG, Anti-inflamatoris, antibiotics, and steroids. Symptoms she listed were: (sample size of approx 16) – OCD – Resolved incompletely YBocs prior at 0, at worst (27-43, aprox median 33) median afterwards about 17. Anxiety disorder – mostly resolved. Range before 0-22, at worst 3-70, and after treatment 0-32, median about 9 Clinical Depression – partially resolved. The numbers not on the chart, but about 8 of the 16 were significantly above where they started after treatment. At worst they were 4X what the normal range is, and at the end the median was around 2x what prior median was. Bipolar – mostly resolved, median at start was about 8, at end about 12, at worse about 25. All 16 were subclinical in the after treatment category (below 25) ADHD – resolved- it looks from that chart like they all went up 4-5 times the before number at the worst – and about 8 of those were in clinical range, but they all but 3 went back down, and those 3 either above clinical level, or just under before treatment. Oppositional behavior – went up 3X the prior rating at worst, and largely resolved (median about 2x the prior rating, but in subclinical for most kids) However 4 kids that were subclinical rated themselves in clinical range after treatment. Response to interventions: 15 kids – antibiotics, more than half - Very much improved, a third improved, and 20 percent or so no change. Anti-inflammatory – 10 kids One kid very much improved. 5 somewhat, 2 temporarily, 2 not at all IVIG – 7 kids 2 somewhat improved 5 very much improved Steroids – 8 kids About 3 – no improvement, 2 somewhat, 1-2 very much, 1 temporary Hornig: Yes – she talked about CLIP. She was pretty amazing. Something I noted when she talked about the mouse study, was that they have to give the mice a drug to open the blood brain barrier, otherwise won’t work. She also talked about Serotonin receptors in the GI track and GI function and sleep. It seems most of current work is Autism. Sorry – didn’t take many notes during her talk and it wasn’t on the CD they handed out (did you think I got all the detailed stuff above from my notes?! – a FEW of the presenters made their slides available on the symposium CD ) She cited the best quote of the symposium. Einstein when he was teaching – A student said “all of the questions on that test were the same as last year”. “True” said Einstein, ”but, all of the answers are different”. Murphy: Mostly talked about antibiotics. I’m running out of steam here, so refer to others notes on her talk. It was good too. I wish there were more time for Q and A on day two. I had to leave for airport – I left during presentation on woman that groups different symptoms of Lyme disease into different categories (we’re talking about very large amount of data from very large sample group). I did have the opportunity to ask about the kids that did the original study with Swedo – and what became of them as adults. She said the all got better. But she believes that they got better because they all got treatment. We didn’t talk about “how much better” – a researcher may think that 20% better is better. She and Cunningham both said that early treatment is important, the longer it goes unchecked, the more difficult to correct. This would consistent with what I heard about the research in the other disciplines presented on day 1. I wish I could convince more people to run, don’t walk, to participate in the study. If any of you are reading this and your child might have pandas - Its your best chance for a full recovery for your child, from the best doctors in the world on this disorder. Get into the IVIG study at the NIMH.

tpotter - Did you catch the name of the Lab that Cunningham is opening - Molecularly Labs or something like that? She didn't really make and announcement - she just said she is starting a commercial lab - but she had a slide with a name. So might be further along that just trying to start it? I wish Cunningham had presented more info on newer stuff. She did say that they ran correlation on about 110? samples and looked for correlations in the antineuronals and symptoms. They only used samples that had clear strep association. I think Anti -Lyso was usually associated with Tics. D2 usually higher for pandas patients. The numbers aren't absolute. But if you are considering ani-phych meds, you might want to look at the Dopamine numbers to see if they are really high and a med that can block Dop might be the way to go. A consistent theme I heard the first day was -and this is for all the other post infectious diseases of the nervous system like MS, Carditis, Lyme - is early aggressive intervention to prevent the disease from moving to either chronic, or in the case of the cardiac stuff - fatal phase. I'll post more later today when I have some time.

-See you all there! kerry

We will probably find each other by Friday morning - but in case we don't or for those coming up on Friday only - how about we meet for breakfast on Friday at 7:45? The agenda says continental breakfast from 8:00-8:30. I just felt like that would be too short. Hopefully the coffee will be ready a few minutes early! I'll put something on the table that says "parents". Looking forward to meeting you all.

I would try : first - Dr. Sean McGhee - pedieatric immunologist. You will need a referral to see him, from your pediatrician or from another doctor. Make appointment through Stanford (Lucielle Packard Children's Hospital). I'd try him first. he can do testing and evaluate. I don't know if he perscribes antibiotics or not. My son is on them, but we get those from another doc. Dr McGhee did IVIG for our son last year. You will want to make sure your insurance will cover it - Stanford must be most expensive place ot get IVIG if you don't have insurance. If you can't get into see him or don't have insurance there - there is a doc teating pandas kids in Petaluma - who I hear has very reasonable rates for ivig - named Dr Sunjay Sweig: Hill Park Medical Center 616 Petaluma Boulevard North, Suite C Petaluma, CA 94952 Telephone: 707-778-3171 fax: 707-778-6744 Office@HillParkMedicalCenter.com for information and to reach the office staff. And Dr Margo Thienemann. She is a psychiatrist. Located near Stanford - depending on what kind of services you are looking for. She gave us our original diagnosis and ran titer test on my sone, as well as will perscribe antibiotics and other meds if you child's case should warrant that. She has a lot of pandas patients in Bay area. Margo Thienemann MD maps.google.com 900 Welch Road #207 Palo Alto, CA 94304 (650) 324-3241 Good luck.

That is an excellent point. Even researchers say that the initial strep episode may easily be missed - and if subsequent episodes are set off by virus or other immune activation - the strep is long gone for many at the time they are being evaluated.

I hate the term "sudden onset" . They need to define a window - my son developed more and more symptoms over 4-5 weeks or so. And how do you say tics are sudden or not. One day he didn't tic, the next day he did. Sudden enough? Click on the "Boy who caught OCD" video posted on the page you reference - it is an interview with Beth Maloney said that Sammy seemed to add more and more symptoms over several weeks. And if you had witnessed a behavior in the past, say, bed wetting, separation anxiety, even a period of ticcing, does it preclude it from being sudden onset? NO! It was probably a minor pandas exacerbation passing for a "normal" phase that lots of kids go through. ITs a subjective term. And it requires the doctors subjective definition, and the parents version of the definition to align to get a diagnosis. I actually almost didn't pursue PANDAS because of this term - I disqualifed my son because for me it didn't happen in a "sudden, overnight" manner. And he'd had some "phases" that were similar before, not exactly the same, and not as severe by any means, but he had had odd periods of separation anxiety and unreasonable fear as well as moodiness and bedwetting. Swedo has said that typically the first episode isn't caught (usually several weeks after the strep infection) . ITs the ones after that which become more severe and closer to the strep infection (or other illness).

JAG10 -- it seems the researchers have enough contact with patients over the past 20 years that have passed puberty that they should have some information on weather it will remit , and what chances of that happening are! There was a 10 year follow up study with pandas patients that was sppossed to published last year - and never got completed (or published). Some of that data must be somewhere.

Im back...twice in one day might seem to indicate I'm slipping back to stage 3!!...but I just re-read "a Way Forward" and yes - Swedo (actually there was a study by Kurlan 2008 - that found found 87% exacerbations could not be found to be triggered by GAS, only 7-25% were caused by GAS, were caused by other things..Im assuming these were not initial episodes. So I guess I'm not alone. I just wonder if those who only have a recent strep infection - no other know infection - are the ones going into remission. The PEX vs IVIG question is a good one - esspecially since if you read the original study, it seems that PEX is better. I do know that the theory is that the donor antibodies will regulate an induviduals production of antibodies longer term (there is a feedback loop where once an antigen is found, the cells ask again and again for that which they can latch onto - teaching the immune system to send out anitbodies immediately when it finds any trace of the antigen. In our kids cases they send out anitbodies very similar to strep antibodies, but that attack themselves). Ill see what she says. I'm hoping to get trapped on an elevator with a few of them...one can dream! I'm planning on switching up the antibiotics. As for IVIG again, not unless we have to, or I hear some overwhelming data that doing it more often leads to better results. DS improved after IVIG for up to 4-5 months, then started to slide back (most notable when sick). DS has EXTREME reaction both times. 10+ days of migraines and vomitting if I missed an adult does of advil every 4 hours (I'm talking vomiting in the middle of the night 10 days after IVIG becasue I thought it was time I slept more than 4 hours!) . Holding his head and screaming. I got and gave steroids the first night when it was extreme - which he threw up. I was petrified. If we do it again I will try doing the steroids before and after for several days.I think Dr B does this. He also has bad needle phobia now, and avoids telling me stuff because he's afraid I'll take him in for blood tests and IVIG. I'm waiting for the sun to go away before changing the antibitoics. DS plays baseball, and got major sun sensistivity on Doxy last time, so he couldn't stay on it. There is some interesting Dopamine, glutamine receptor info on page 323 of "a way forward". Don't know how that might relate to the methylation cyndilynntk, but I think I've read somewhere it is connected.

HI all, I've been around the board here for a couple years. I've gone through what I consider to be the "Five Stages of ACN" - 1) Lurker 2) Sharer 3)Addict 4)Complete Withdrawal (I was spending too much time here, and I didn't see my son get 100% better-so I felt like I had no business advising others) and finally, 5) Healthy Relationship. I mostly read and only reply if what I have to say is different from other posts, and I only check in once a week or so. I'm preparing for two things - one is attending the symposium in TX , the other is taking the next step in our search for full recovery. They are basically the same thing. Right now I've got some words written in no particular order on a sheet of paper. I plan to review all the literature in my very thick file of research -so I have a shot at understanding some of the presentations! I'm hoping that some of you out there have similar questions and can help me formulate these questions, and perhaps prioritize (if I even get to ask any). I'm sure I'll be posting any new information I glean from those two days. My son has PITAND, sudden onset after a strep episode (although we don't have documented rise in titers - tested too late) . We've had two HD IVIGs of 1.5mg, 9 months apart, and are currently 6 mos. past the last one (April 2011). They have had a tremendously. The first was more dramatic improvement, but he was sicker. Unfortunately for us IVIG was not the lasting cure we had hoped for. He seems to improve steadily for several months, then decline somewhat slowly – especially if he catches a cold. We are going through that right now. I don’t know if it will be a few days or several weeks, but the symptoms have come back (not as bad as before IVIG-but there). Most of my questions are centered around this. I’m not planning on asking most of these OUT LOUD, I’m hoping most of the answers are in the presentations, or clues to my answers are there. I’m just hoping for something to direct to our next best step with DS. Chronic Pandas- Can going without treatment for too long damage the immune system so it never figures out how to fight off viruses without creating anti-neuronal antibodies- even after IVIG? PANDAS v PITAND -Have you found any differences between Pandas and Pitand kids in terms of infection, immune issues, or success with different treatments? Chronic Infection – are some of these kids infected with chronic strep, or other infections – causing immune “confusion”, which leads to “chronic pandas”? Lyme- in the current study the kids had to have a very close relationship to strep, and I understand they were also screened carefully for lyme. What percent actually had Lyme (I heard those kids were not allowed into the study). Were they screened for other infections (like mycoplasma pneumonia) or immune deficiencies? IVIG -What makes some kids better after one round of IVIG, and other not? Is there any evidence that several IVIG’s done closely will have better result? Any evidence that 2 is better than 1.5 (and what about low dose – why doesn’t that work?) Antibiotics – this is more of a personal question, not one I think I’ll find an answer for at the symposium. I’m planning on switching antibiotics again. Doxy or Augmentin XR. The XR – I’ve seen a number of posts on successes with that. Doxy, because my son MAY have mycoplasma or Lyme, and Doxy better for both of those than the Azith DS has been on for almost 2 years…but can’t take Doxy in summer because of sun sensitivity – so I’ve been waiting. ANY thoughts or input on above appreciated. What else should I be considering as I sit and listen? PS – I tried giving DS some Delsym yesterday and this morning and it seemed to help a bit. He has mild sniffles, and we saw an uptic in symptoms past few days…not sure it’s better than Advil yet, but appears at least equal (could be placebo effect I admit – but he said it helped). Thanks to whoever posted that one!

Might also want to get pertussis titer done if your state requires DTP booster for school . If your child makes the antibody - you don't need the booster and your doc will proably have no problems writing a letter for you.

Got my pandas son a full "twice exceptional" evaluation around the time of pandas DX...discovered unable to do spatial processing at same time as fine motor. There were 2 tests that tested for this specific thing. He was at bottom 2% on one, and maybe 10% the other. He did very well on everything else. You need this in school to "show your work" when doing math. Copying from the board (or copying anything - in you notebook from a page, especially graphs/pictures). I think it probably effects spelling for some kids because they need to "see" it in their heads- ( you know how you write a word and it doesn't look right?). My son's spelling was never really effected - but I think he's learned certain compenstion skills. He can do very complex math in his head - we thought it was because he's smart - but its because he has no choice but to keep it all in his head because he CANNOT write it down at the same time ! I had no idea there was a specific area of your brain where these two functions overlap. Imagine the stress of being asked to do something so simple that everyone else int he class can do it with ease, but you can't do it at all - at any given point in the day! I would get you child evaluated and get him using an alphasmart or keyboard of some kind if you find the same deficiency. That was recommended for my son (as well as support with anything that had to be copied - hard copies of anything put on the board by teacher, and copies of notes taken by other students in class) but he refuses, becuase that was at the start of middle school and he didn't want to be different. Maybe if we knew earlier we could have helped him do/feel better about his work and most importantly avoid all that stress. Good luck!

Thanks LLM that is interesting. I will read-up on it. My son did come up deficient on zinc a couple years ago, which sent me to gastoenterologist thinking he was perhaps celiac. She did a different test and he was in normal range on that, and said that kids zinc fluctuates alot with growth, etc...but always made me worry a little, also def ferretin. Another mineral seems not absorbing - getting plenty in diet. I did supplement a Little zinc for a while (under docs supervision) - bu DS hated taste - and I didn't seee any difference.

what is KPU ?- I just tried to google it, but didn't see any obvious meaning for the acronym. thanks-

I've read that Doxy is preffered from mycoplasma, and it could take 9 months of treatment to see it subside if it is a chronic infection. Also, its treated a little like Lyme with antibiotics cycled off for a couple weeks after 4-6 weeks on. High IgM means it is active, recent infection- I gG can stay high for long periods of time after an infection has subsided. BUT, that IgM is not likely to rise AT ALL on subsequent infections. So an IgG that is trending upwards would indicate the infection may still be active. I don't know how much of a raise would indicate that I'm sure there is some allowable delta for samle/daily fluctuations. Your sons look like they are going up steadily. Kimballot is right - Mycoplasma is a Lyme co-infection, but its also "walking pnemonia" - its everywhere. I did a bunch of research on this after I found my son's IgG was 25,000, IgM normal. YOu will find conflicting data and opinions. Doctors are taught to look for the IgM - but I've read at least one study that found that IgM usually only goes up the begining of the FIRST time you contract it. Does your son have any "regular" symtoms (upper respiratory infection, persistent dry croupy-like cough?) DUT- I didn't know that about selenium - very interesting!