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Buster

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Posts posted by Buster

  1. EAMom sent me a reminder about this post and in light of the recent presentations at the IOCDF, I thought we should pick this one back up.

     

    What the heck is sudden onset?

     

    If I were some researcher who didn't believe in PANDAS, I'd wait until this was the new established "criteria" and then attack it as "ill defined" and then prove it didn't occur because the kids in my sample who had onset overnight, didn't separate from kids who had onset over a week. If you wanted to be a PANDAS-naysayer, nothing is easier than to attack definitions.

     

    I look at Kurlan's 2008 article where he painstakingly says that he met the published criteria of 1998 -- did he meet the criteria of Swedo's 2004 "separating fact from fiction" article -- nope -- he stuck with the original definition and attacked episodic.

     

    I think Swedo and Murphy and others are going to have to publish something much more precise to get around this.

     

    Here's my try (this is just a draft to get your comments):

     

    "Sudden Onset means a change of symptoms from a baseline of functioning behavior to an inability to function over the course of 1 month or less. This abrupt change of behavior may be measured using standardized instruments such as a change in CYBOCS of +16pts. A change of 16 pts represents a dramatic shift in symptom severity from a child who was functioning (perhaps with some quirky behavior/compulsions) to one unable to function (fairly constant imparement, "possessed", everyone on eggshells, unable to function in a school setting)."

     

    Here's a try at a graph:

    SuddenOnset.jpg

     

    And for relapsing/remitting:

     

    RelapseRemit.jpg

     

     

    Thoughts? I realize a lot of cases may not meet the above. But does the above help better than "sudden onset"?

     

    Buster

    edited based on comments below from Vickie and EAMom.

     

     

    sudden onset is too subjective. More importantly - if you catch your child early in mini-exacerbation, as described by Murphy, or, at early stages of VERY first episode, where strep may be months prior to the first symptom, your child will go untreated, they don't meet the pandas criteria. And, unteated strep, untreated pandas, is not going to make it easier to treat next time.

  2. What we did see was a dramatic falloff of symptoms post-IVIG for approximately 6 months. Then when there was a fever, symptoms would return. Not disasterous like the last time, but say 40-50% of last time. These would subside, but there was a baseline drift. I guess the way I'd say our case went was if 100% was the worst, we got about 90% back when daughter went on azith, then when got sick again, baseline moved up to about 20% (i.e., 80% better than worst). Then sick again, baseline moved up to 40%. We did IVIG again, returned to about 10% for about 6 months. Then when sick, baseline shifted up again.

    I'm sure you all have checked for other co infections because you have so involved with all of this research through these years. ... How is your DD now? Will you be doing more IVIGs? Is she still on Antibiotics?

     

    Our history is that March appears to be the bad month for us. We think this is because dd11 gets sick in February.

     

    We will likely do another round of IVIG as we've had good results from prior IVIG's (one in 2009 and one in 2010). In the prior 2 IVIG's we saw 80-90% improvement. This is roughly similar to the results in some cases of Swedo's original study where she found children with acute symptoms and PANDAS consistent OCD symptoms had a 58% improvement one month out from before treatment and a 68% improvement one year out(i.e., this was by no means the cure-all, but there was sustained improvement in these very acute children).

     

    One of the better papers (meaning understandable) on why IVIG likely works is here : http://bloodjournal.hematologylibrary.org/cgi/content/full/115/9/1663

     

    My summary of the paper is that they think IVIG works by either:

    1. Saturating all the Fc receptors on the APCs so APC never presents the auto-antibody
    2. Binding to a suppressor mechanism (currently unknown) that prevents the APC from presenting any auto-antibodies
    3. Binding to Fc receptors on the endothelial cells so auto-antibodies have no place to attach and die

     

    I think it is (a) -- namely that the APCs are saturated and never get around to presenting the auto-antibody and hence the cycle stops -- but who really knows.

     

    On the concept of co-infection, there's a lot to consider there. The literature seems quite compelling that Sydenham Chorea is a sequela to an untreated GABHS infection. There's something going on when the immune system can't clear the particular antigen. Perhaps this is what is happening in Lyme too -- the original antigen just can't be cleared. Perhaps it isn't co-infection as much as an inability in some people to clear the original antigen. The immune system does strange things when it goes into "backup mode".

     

    If we think that PANDAS is similar to OCD sequela in Acute Rheumatic Fever, then it is likely that PANDAS is a genetic disorder. Apparently about 3-6% of the population is genetically succeptible to ARF/SC. Beyond this genetic predisposition, they need the right strain, they would need to go untreated for GABHS, and about 30% of those would get ARF and about 20% of those would get OCD and/or SC.

     

    We do keep our daughter on prophylactic azithromycin, but have concluded that this at best minimizes the reaction but does not stop an infection or reaction. Antibiotics don't kill bacteria, they just help the body's own immune system kill the bacteria. So what we think is happening is our daughter gets colonized when exposed to GABHS, her body has an immediate response and produces the antibodies and the cycle begins.

     

     

    Buster

  3. Hi 3boysmom,

     

    SS8 has tics but no OCD - treating with low prof dose antibiotics, DS 10 -titers keep rising (now 1920-which is where his brothers were when he woke up different) but not big issues & treating with prof antibiotics.

    So DS11 is on Augmentin XR 1000mg twice a day. Did you put DS10 on anything?

     

    I just want to say that DS11 is MUCH better than 2 years ago, but still not back to himself. We struggled with the choice of where do you say good is good enough and be happy with the progress that you have or as he gets older are we missing the opportunity to completely heal him. We are just worried that the IVIG will bring him back to the scary stage and he will not return & neither will we for hurting him.

     

    This is a big decision and we too went for IVIG after the scary symptoms returned (in our case the eating disorder). I will tell you the first two weeks after IVIG were particularly difficult and made us wonder if we had made a horrible decision as almost all behaviors returned with intensity for those 2 weeks.

     

    Dr. K often says in his talks that the predinsone is there for the parents - to help them understand that it is an autoimmune disorder. In our case, our daughter was exquisitely sensitive to her sister getting GABHS. In fact when PANDAS daughter ramped in symptom we could invariably take younger sister in and she'd be culture positive. When symptoms subsided, we could take younger daughter in and she'd be culture negative.

     

    We decided to call this the "peanut allergy" equivalent. She just had to be around someone with peanuts to have a reaction. (I know, not very scientific, but what we observed).

     

    DS11 began the constant questioning and hand washing, later that day kid goes to doctor...Strep!

     

    Yup. We've seen exactly that.

     

    We are hoping the IVIG with boost his immune system and this will not continue to happen.

     

    That hasn't been our experience I'm sorry to report. What we did see was a dramatic falloff of symptoms post-IVIG for approximately 6 months. Then when there was a fever, symptoms would return. Not disasterous like the last time, but say 40-50% of last time. These would subside, but there was a baseline drift. I guess the way I'd say our case went was if 100% was the worst, we got about 90% back when daughter went on azith, then when got sick again, baseline moved up to about 20% (i.e., 80% better than worst). Then sick again, baseline moved up to 40%. We did IVIG again, returned to about 10% for about 6 months. Then when sick, baseline shifted up again.

     

    We don't know how others have done, but that's what we see.

     

    Buster

  4. Yes, the underlying drug used is amantadine, an N-methyl-D-aspartate (glutamate) antagonist. They found in http://www.springerlink.com/content/724p204w617032k7/fulltext.pdf that the drug provoked a selective enhancement of noradrenaline plus a minimization of adrenaline, dopamine, plasma serotonin and platelet serotonin circulating levels. Still trying to figure out the study and what else might be going on.

     

    Buster

  5. Hi Beeskneesmommy

     

    A number of items in your post. You might want to take a quick look at the 2008 thread: http://www.latitudes.org/forums/index.php?showtopic=3756

     

    which tries to explain some of the research around ASO and Anti-DNAseB.

     

    The only properly studied effect has been rising ASO or rising Anti-DNAseB. If you have chronically elevated or falling titers, then basically nothing is known. It literally is not studied how long it takes for these antibody levels to fall.

     

    When the titers are rising, it means that the child had a strep invasion 4-6 weeks prior (ASO rise) or 8-10 weeks prior (AntiDNAseB rise). However, studies indicate that ASO rises in only 54% of the children with confirmed GABHS colonization. Even when adding in AntiDNAseB titers are confirmatory in on ~70% of cases -- meaning ~30% don't show such a titer rise.

     

    When we ran our informal (ala non-scientific) study on ~400 children on this forum we found :

    • Only 15% of girls had elevated ASO or Anti-DNAseB over the course of the illness
    • Whereas 54% of boys had elevated ASO or Anti-DNAseB
       
    • In addition, 23% of girls did not have a rise in ASO or Anti-DNAseB despite a positive throat culture
      whereas 14% of boys had this situation.

     

    What I found interesting was that boys appeared ~4x more likely to have a rise in ASO or Anti-DNAseB

    Whereas girls were ~2x more likely to be labeled as "carriers"

     

    (see http://www.latitudes.org/forums/index.php?showtopic=9495&st=0&p=79704&fromsearch=1entry79704)

     

    I was also wondering if you had been on amoxicillin in your time of elevated titers. Could you provide what antibiotics you tried?

     

    Best regards,

     

    Buster

     

     

    Hi:

     

    I need some help understanding this. Since last June, my son (4) has had ASO of 400+ and DNASE in high 900's. He had Strep titers tested June 2010, Sept. 2010, Jan. 2011 and last week, May 2011. He started BID antibiotics last Sept. 2010, which did not seem to make a dent in the titers, in fact, his last DNASE, last Jan., actually went up. Sooo, now, about 4.5 months later, his titers are ASO 105 and DNASE 159. I am not looking a gift horse in the mouth. It is true that his PANDAS symptoms were almost non-existent from last Jan - the end of last March, likely due to starting a diff. ABX called Cefdinir. However, recently I have noticed that some of the symptoms, especially during an illness in the beginning of May, were returning. The most recent symptoms were accompanied by a fever and sore throat and I felt sure from my observation of his behavior that he had Strep. Throat culture was neg., and apparently correct if you go my the titers. Can anyone shed some light upon PANDAS symptoms seeming to return even thought titers have decreased significantly?

  6. For the first of your questions, you might find this thread helpful.

     

    http://www.latitudes.org/forums/index.php?showtopic=7855&view=findpost&p=63932

     

    The referenced paper is quite good.

     

    Buster

     

    Just looking for info or links for

    1. sources on how IVIG works in the cells for a PANDAS child and how it changes their behaviors.

    2. Time it takes an IVIG treatment to work in the PANDAS child's body.

    3. what happens if a health child get IVIG, any symptoms?

  7. This is super tricky to do (especially with someone at 12). In the discussions with our daughter, she referred to the OCD symptoms as part of her -- helping her do things. It wasn't until she got better (and got older) that she had the insight that something was off. When she was no longer exhibiting symptoms she was able to reflect back on the time and say "it was something I sort of wanted to do and then it got away from me" (referring to an eating disorder). When reflecting back on the defiance and outrageous demands, she'd say "it didn't seem weird when I was doing it... it does now." We did do some video taping and then when she was in remission showed her some of the videos. This was effective at showing it and being able to talk about the behavior.

     

    At 12, she might not be willing to admit anything is amiss (certainly not to parents) and so you might consider having a neutral confidant involved (such as a psychologist/phychiatrist) or even an journal.

     

    Best wishes,

     

    Buster

     

     

    My now 12 year old daughter has just been diagnosed with pandas/pitands. We have just consulted with Dr. T and he has put her on a course of antibiotics. I tried to talk to her about why she is taking the medicine. She again denied that anything was wrong with her. It is so sad and frustrating. She once was a very articulate, vibrant 10 year old girl and now her appearance is odd and disturbing and all along even in the most bizarre of her actions she acts like nothing is wrong. Does anyone have any advice about how they communicate hope and reassurance to their child? I know my daughter is suffering but she won't acknowledge anything is amiss.

  8. I can't see the original email, but if I were replying to a letter about de Oliveira's paper, I'd probably say something like the following:

     

    Thank you for sending me a copy of the most recent de Oliveira's paper. I wasn't sure if you had read her prior paper (
    ) in which she correctly states that about 40,000 children die each year of
    untreated
    streptococcal infection (with another 2 million needing heart surgery).

     

    Thank goodness that despite her comment in that previous paper that the "the pathogenesis of RF remains elusive [and] how and why a small percentage of patients develop RF is still under investigation" that children can still receive treatment for a GABHS infection and prevent acute rheumatic fever. Based on the efficacy of antibiotics for RF, it would be immoral to withhold treatment pending the outcome of researchers trying to discern the pathogenesis of the disease.

     

    This is at the heart of the debate about PANDAS. No one debates the clinical signs. To have PANDAS one must have a diagnosis of OCD or a tic disorder -- this is the first criteria. No one debates the apparent efficacy of the Perlmutter treatments. What is being debated (just like for Sydenham Chorea for the past 200 years) is whether the symptoms are caused by group A beta-hemolytic streptococcus. Luckily recent studies such as that by Kirvan are helping us understand both Sydenham Chorea and PANDAS (see
    ).

     

     

    this might get her to read the actual cunningham paper :-)

  9. I've been thinking about how to respond to the post. I deeply understand the frustration you must be experiencing. Some comments however,

     

    For the iep, are you pursuing eligibility under OHI or under SLD?

     

    If OHI, then the required items is to have a condition and show it is negatively impacting access to the educational program.

     

    Under current definition, someone identified as being on the pandas cohort would have either OCD or tic disorder. It is irrelevant (for purposes of the iep whether the team agrees on the cause of the symptoms - only the symptoms need be present). As such you may find it easier to get a dsm vi diagnosis of anxiety disorder or OCD or tics. Tourettes syndrome is typically classified under OHI even though the definition of ts exclude medical cause.

     

    The real hurdle you have to pass is not what to call it, but showing it is impacting access to the educational curriculum and by reason thereof requires special education.

     

    I know first hand how tempting to try to convince others of pandas, but that's unlikely to be your best route.

     

    No one disputes that children diagnosed with pamdas have profound symptoms, the only dispute is whether GABHS is the culprit. Focus in the iep on the symptoms and not the cause and the least restrictive environment that will help you child access the cirruculum.

     

    I know you'd rather dump the papers on the nurse, but just switch it around and say "you know the controversy is about the cause and not about the symptom right?"

     

    Buster

  10. Sudden onset OCD is present in about 70% of children with Sydenham chorea. In Swedo's studies in 1994-1998 some children with sudden onset OCD had the episode 3 weeks before Syndenham and some 3 weeks after the movement disorder.

     

    Strangely having Sydenham Chorea diagnosis may actually help you in getting treatment. Many believe that Sydenham Chorea is monophasic (and it is in about 70% of cases), and many believe it is self-limiting (which it is for the motor abnormality), however, there are very spread and inconsistent results for the OCD accompanying the SC. van Immerzeel's paper http://www.ncbi.nlm.nih.gov/pubmed/20349351 on the benficial nature of IVIG for SC.

     

    There are also many papers from Brazil as SC and SC+OCD are quite a problem still there.

     

    Best regards,

     

    Buster

  11. Interesting question... We're doing well and I'm not on the forum all the time. When I do check in, there's a lot of great advice and I'm finding I don't have a lot to add -- this is frankly a bit of a relief.

     

    Back in 2010, I started documenting everything I had collected or learned in hopes that I'd save someone the hours I spent searching.

     

    I hope these resources continue to be beneficial and I update them occasionally.

     

     

    Buster

  12. I believe that the above statement (about carriage not being as b-9 as once thought) was based on personal communication with Ed Kaplan (WHO strep expert). Maybe Buster will offer more info.

     

    EAMom is correct. The original comment came from a discussion with Dr. Ed Kaplan regarding research he has been doing for well over 20 years on carriage. A good paper on the topic was the Th17 activation in nasal innoculation/colonization in Cleary and Wang's recent paper. See http://www.pnas.org/content/early/2010/03/11/0904831107.full.pdf

     

    This is one of several papers that are looking at the effects of carriage (in this case in mice). There's a lot of distance between mice and men, but this is part of the research that is looking at the immune systems response to just carriage.

     

    Regards,

     

    Buster

  13. Buster---as for the "specific tests for antineuronal antibodies"--are you talking about the 4 that Cunningham tests for, or some of the others that have been tested by other neuros??

    Just hoping that over the next 5 years we get more science in place that makes something a better test. I think Cunningham's are the leading candidate, but Dale and Church also had some ABGA tests. Bottom line, hopefully something better comes along :-)

     

    Buster

  14. So bringing this full circle back to the article :-)

     

    I think the article and ones like it will be used to say:

    1. The definition of PANDAS is too broad as currently written and includes kids who do not have the disease
    2. The evidence for assertion (1) is going to be Kurlan, Singer, and now Leckman's papers where they will show that Tourette's Syndrome kids meet the "previously published criteria of PANDAS" even though they don't have the explosive OCD symptoms.
    3. The neurologists will save face saying "we weren't arguing whether kids had auto-immune triggered OCD" just that the definition was too broad. That's all we were trying to say (yeah, right....)

     

    I also think the following things are likely to occur over the next 5 years:

    1. New studies will focus on the original explosive OCD trait and the cooccurance of other psychiatric conditions
    2. This will tighten the criteria and neurologists will feel heard and Swedo will be vindicated/proven
    3. There's likely to be some fight on whether PANDAS is a mild form of Sydenham Chorea and whether Sydenham Chorea should be allowed to be a standalone diagnosis for Acute Rheumatic Fever, but that's the fight for the DSM-VI book.
    4. Doctors will switch from testing unreliable ASO and AntiDNAseB titers to using symptoms and specific tests that check for anti-neuronal antibodies.
    5. It will become common practice and the AMA will recommend that throat cultures be given anytime a child presents with explosive OCD traits (and regressive behavior)

     

    Okay, the last 2 are just things I wish for, but I can see happening within the next 5 years.

     

    I truly think we'll see a whole bunch of these "repositioning papers" where the abstract is of the form "did not confirm existence of ..." and then the details of the paper will talk about the paper being "underpowered for OCD-only" or "selection criteria used the 2002 criteria rather than the revised 2005 criteria" or "that we found one case fitting the definition in retrospect in our control group indicating that the admittance criteria needs to be fixed". This posturing will happen over the next year as the evidence mounts. Bottom line, this will resolve. We're just likely to face another 5 years of the war until the original Perlmutter study is redone.

     

    Buster

  15. Quoting from the study:

     

    "All subjects were sequentially enrolled at one of six clinical settings( Yale University, Cincinnati Children's Hospital Medical Center, New York University Child Study Center, Johns Hopkins University School of Medicine, University of Alabama at Birmingham, and University of Rochester School of Medicine) during a 4-year, 6-month period from July 2002 to December 2006."

     

    The diagnostic criteria used was the one from Swedo's 1998 paper on the first 50 cases (i.e., Swedo's clarifications from 2004 and 2005 on episodic course, co-occurent psychiatric conditions, and acute and dramatic onset were not used).

     

    In Table 1, 26/31 proported PANDAS cases had a diagnosis of TS (inclusive of chronic tic disorder). 49/53 had such a diagnosis in the non-PANDAS cases. To have a TS diagnosis required vocal and motor tic with no remission lasting for > 3 months.

     

    22/31 had OCD in the proported PANDAS group (but this is co-occuring with TS) and 35/53 had OCD in the non-PANDAS subgroup (with the same coocurrence with TS).

     

    You'll see that there could be only 5 OCD-only PANDAS cases and only 4 OCD-only controls.

     

    As such, the study is underpowered to reach any conclusion regarding OCD in the absense of TS diagnosis.

     

    Buster

     

     

     

    Buster, Gilbert had 6 kids he felt had pandas in 2005. R u saying all these kids were from 2002? I know Gilbert serparates his pandas from his TS. R u sure these were TS only kids cuz in cincinnati there were definate pandas kids around Gilbert and diagnosed as such in 2005.

  16. What happened to Do No Harm? If a dr tells a patient, "your child need antibiotics" yet does not give them antibiotics, they are doing harm. I am not turning this into a bash the doctor thread, but quite frankly, my patience has run thin. I don't see how a physician can justify that to himself or his patients.

     

    Colleen

    There's a lot here that I could go into, but the short comment is that it appears that by the time the report got back to the doctor (i.e., throat culture positive) and this got back to the parents -- enough time had elapsed that the children were already "feeling" better and didn't get antibiotics (i.e., this is largely the parents choosing to address or not). I'll have to go and see if I can find the original clinical trial invite as I wonder what parents were thinking was going on when they signed up.

     

    I'm pretty sure if I was part of the clinical trial and heard my kid had a positive throat culture, I'd be getting antibiotics :-)

     

    One other thing to consider is that the whole longitudinal study and data is the same set of kids that Singer, Kurlan and Kaplan were all writing about in other papers. The same methodological flaws that existing in the original sample group, exist here. Essentially if you wanted to know if GABHS caused exacerbation in OCD-only cases this study tells you nothing. If you wanted to know if GABHS caused exacerbations in long established TS cases, the studies tell you something. What you really get is that:

    • if you pull a kid from the Tourette's study group -- it'll likely be a boy
    • if you pull a kid with established tics -- exacerbations will be due to lots of things
    • if you pull kids with a baseline CYBOC score > 16, these will fluxuate about 5-10 pts over a year
    • if you ask tic folks to evaluate OCD, you generally don't have them recording anxiety or other comorbidities
    • once a study is conducted with the term PANDAS and non-PANDAS - those terms will stick even if the kids don't match the actual PANDAS criteria upon reflection (rather than at time the study was constructed). Remember these kids were recruited in 2002 before the clarification by Swedo in 2005.

     

    Sigh.

     

    Buster

  17. I've done a first pass analysis on the paper and the cited references (particularly reference 47, Lin et al Sept 2002).

    1. Lin's criteria is being used to define an exacerbation. If taken at face value, this means an exacerbation is:
      • a 7 point rise in CY-BOC score with a minimum value of 16
      • or a 9 point rise in YGTSS score with a minimum value of 19
      • or a combined rise of 10 points with a minimum value of 33 on a combined CY-BOC and YGTSS score

    [*] This is important because the sample group was drawn from the Tourettes study group. This means that most of the population were patients with Tourettes or chronic tic disorders and had had such a diagnosis for some time.

    [*] In addition, the sample was prodominantly male (i.e., 81% of PANDAS cases were boys)

    [*] Only 5 proported PANDAS subjects and 4 non-PANDAS subjects had OCD-only symptoms. This implies the study is underpowered for any comments on OCD-only PANDAS presentations.

    [*] The paper correctly highlights that many of the proported PANDAS patients would not be considered PANDAS if the criteria was tightened to include Swedo's observations in 1998, namely the co-occurance of anxiety, emotional lability, irritability, aggressive behavior, sudden difficulties with concentration or learning, developmental regression, etc.

    [*] As others have pointed out, the blind was broken in terms of the results of GABHS throat cultures. What was good, however, was that the study did track whether antibiotics were given. On the other hand, the duration, compliance and type of antibiotic, however, was not tracked.

    [*] There is also a reference to the non-proported PANDAS that seemed awfully PANDAS-like in retrospect. This is likely what prompted the researchers to say that perhaps their admission criteria is flawed and needs to be tightened.

    [*] The duration of the exacerbation is not listed. Lin notes in the 2002 paper that the duration of OCD exacerbation was approximately 3 months.

     

    So, what is the core take away from this study. Well, I think the core is

    • the high degree of agreement on what is an exacerbation
    • the improved clarity that Tourettes (i.e., long term tic disorders that do not have remission) is unlikely to be PANDAS
    • continued confusion on what means "sawtooth". Leckman and others are using an increase of 7 points on a base of 16. In looking at CY-BOCS, this appears to be a change in 2-3 questions by one category (please help me folks if you know the CYBOCs score better). This is actually a relatively minor change relative to the explosive change reported by Snider and Swedo.

     

    I appreciate that the paper will be used by many to say "more proof PANDAS doesn't exist" but I think the actual item is more "if you pull samples from Tourettes Study Group, you are unlikely to get a PANDAS kid".

     

    Anyway, that's my first pass response on the paper.

     

    Buster

  18. I agree with all the other posters.

     

    The clinical presentation is the most important. All the other tests (including cunningham) just help round out the picture. ASO is at best a coin flip. AntiDNAseB has a very fixed time window and rate of fall is not known. Igg helps with identifying an immune deficiency, but PANDAS isn't an immune deficiency in itself -- the immune system (if anything) is overactive.

     

    with you the best,

     

    Buster

  19. Hi folks,

     

    I could sure use help from those who have been through IEPs (or know someone who is a good advocate).

     

    Our dd10 has an IEP with OHI for social anxiety, OCD, Developmental Coordination Disorder, and Learning Disorder NOS.

     

    Although she is almost 95% back in terms of behavior, she has several very specific difficulties that are essentially lost skills. These are skills typically learned in 2nd thru 4th grade (i.e., the time of the PANDAS crisis and recovery). Curiously these skills are also ones that require good coordination of the basal ganglia.

     

    The skills lost are in penmanship, math fact memorization, capitalization, spelling and vowel controlled /r/'s and /s/ articulation. She had extreme social anxiety that made it quite difficult for the school to 'pull her out' to work on the lost skills because that pull out was exactly the spotlight of attention that was so devastating to her (due to the social anxiety).

     

    We were able to pull her out for speech because other kids in the class were going to speech as well (i.e., she didn't feel different by going). We just couldn't get her to the resource room for anything else. This basically meant that her IEP goals ended up being around speech with a goal to try to get her comfortable with going to the resource room for math/spelling. Only the speech goals were met.

     

    When we went for IVIG in May 2010, the social anxiety dropped considerably and her mood and comfort with others got much better; however, she still does not want to be pulled out for additional resource help. In some ways this is more a memory of a prior fear than actual fear.

     

    Curiously she's willing to "assist" in one of the younger grades (and learn in the process). We tried this last year and it worked well. It's a perception thing. She says when she goes to the resource room she feels dumb, when she goes to the younger grade to help, she feels like she's stealth learning (and helping). It makes her feel good and helps her self-esteem.

     

    I'd like to write in this year's IEP goals about learning her math multiplication table and improving her handwriting and would even like the method to be through "assisting in the lower grades". I think the handwriting will actually help her spelling and line up her math. Curiously she can easily do the steps of long division, but just can't remember what 4x4 is. We've been using accomodation thus far (i.e., use a math multiplication chart and this has helped).

     

    So, any thoughts about writing into the IEP a goal about learning the multiplication tables or being able to spell 3rd grade words (she's in 5th grade). I live in a bit of worry about causing her more stress, but also know that without relearning these skills she's going to have a very hard time in middle school. I'd like to get the goals identified and then determine if the method is to try using "helping in another class" rather than going to the resource room.

     

    Mostly seeking comments from folks who have been there. The IEPs are always a slightly stressful time with the school.

     

    Best regards,

     

    Buster

  20. Even after IVIg (although only 8 days ago), my ds12's obsession with his "fat body" is getting worse. His PANDAS doc is concerned now, and wants him evaluated as well by the OCD clinic director at UCLA. He is not avoiding all food, but the obsession is getting exhausting for both of us. It starts upon waking, and ceases only when he goes to bed. Doc says he doesn't see this with other PANDAS, but then again doesn't have very many.

     

    Does your child have/had this?

    Did you resort to pharmacological help as well?

    Did that work?

    Did high dose IVIg stop it?

    Did low dose IVIg stop it?

     

    My son had low, replacement IVIg only- wondering if I should push for high dose next time.

     

    Starting to panic now...

     

    Hi Phasmid,

     

    Our child (at the time 7 years old) had compulsive questioning around food and food facts. She started with "will this make be gain weight?" "will my arms be bigger than my sisters?" "does this have fat in it?". This then turned into restrictive eating so that when she did eat she "wouldn't weigh more than 50 lbs". In her case, she had an obsession around not weighing more than 50 lbs. There was nothing rationale here. She was outright paniced and couldn't quite express what would happen if she did weigh more.

     

    She had body image issues with odd measurement rituals trying to prove to herself that she hadn't gained weight. Her pictures and drawings became quite odd with strange proportions. This got so bad we had to hospitalize her for malnutrition because she had lost 15% of body weight in 2 weeks.

     

    It sounds like your son has a very different presentation (i.e., not the restrictive eating, but the compulsive questioning).

     

    We did three things that helped our daughter:

    1) 10 days of augmentin

    2) We got food into her using pediasure and calling it "medicine"

    3) We put her on a lowdose SSRI

     

    I know we changed three variables at once, but the combination helped -- who knows exactly which was the trigger. It sure seemed to be the augmentin, but the SSRI and food probably helped too.

     

    We tried upping the SSRI and that was definitely a mistake as she had activation. We dropped that back down and we were back to contamination fears and restrictive eating again. We switched to a different SSRI (low dose) to soften withdrawls off the 1st SSRDI and that seemed to help a bit. Then we switched from augmentin/amoxicillin to azith and had dramatic improvement.

     

    It's hard to know which combination of stuff helped - i.e., delayed response to augmentin, getting food in her, the delayed response to SSRI, or the nearer term effect of azith, but she had dramatic improvement on the 9th day of azith.

     

    My point is that the body image issue went mostly away. This is over 2 years ago. The restrictive eating had a resurgence about a year ago and we did decide to try HD IVIG and this resolved symptoms.

     

    Not sure whether our case helps you any, but yes, body image questioning is a standard/common OCD trait. Restrictive eating is deadly and scary.

     

    Wishing you the best,

     

    Buster

  21. All I was meaning was that while a rising titer could mean an active infection it also can mean that there was a past infection. Both are possible. In most kids, the infection is cleared on 10th day with antibiotics, and in ~70% of cases, kids will clear on their own in 14 days with or without antibiotics. However in about 30% of cases, kids won't clear without antibiotics. In about 10% of those cases, the strain of strep is a rheumatic strain and in about 4-6% of the untreated cases the kids get acute rheumatic fever. If you take the US population of kids 5-12, this is about 42M. So we're talking ~168,000 potential cases in the US of ARF. About 30% of those get Sydenham Chorea, so the estimated amount of SC is around 50,000 cases. Of that around 70% get OCD, so that's about 35,000 cases of OCD fo the rheumatic strain version. PANDAS may be the same strain or different, we don't know.

     

    Buster

    Hi Buster. Thanks so much for your help and information on this forum, you have been so much help to all of us. I'm sorry if I maybe misquoted you or misinterpreted your work. I was looking at your post from August 24, 2008 on "A little bit about ASO titers." On page 2 under What does this mean summary, "a rising ASO titer (regardless of absolute value) is an indication of GABHS strep; however, you need a baseline to be sure it is rising." I found too (thanks to your help) a medline abstract, "The human immune response to streptococcal extracellular antigens; clinical, diagnostic and potential pathogenetic implications." it stated , "the analyses clearly document in some instances for the first time, that an increase in antibody titer more accurately defines infections than does an absolute titer (eg. "upper limit of normal"), that antibody titers can remain elevated for man months even without GAS, and that some individuals may harbor GAS continuously for months or years without symptoms of infections and without an associated immune response." This was by Dr. Kurlan and Leckman and Kaplan too. My older son has strep pneumonia so I'm not sure how, or if it is playing a part in my PANDAS son recovery. I am assuming it is because Dr. K and Dr. B have family members titers checked. Dr. B. said any "exposure" to PANDAS kid to anything is like putting wood on a fire that you are trying to put out for these kids.

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