Buster

A comparison can be found at: http://www.ashp.org/s_ashp/docs/files/DSho...pdatedDec07.pdf Essentially the big difference is the amount of sugar in the Gamunex versus gammagard. People on the forum have reported similiar efficacy with slightly higher headaches being reported with gammagard (at least from the local sample). Dr. K uses Gamunex. Buster

There seems to be confusion about dopamine and epinephrine in the blood versus what's going on in the basal ganglia. The area of concern for dopamine in PANDAS, OCD and tics is in various parts of the basal ganglia. You can't easily get near that part of the brain or see what is going on there, but what Church, Dale, Kirvan, etc did was take cell lines from neuroblastoma cells and then see whether antibodies in the blood interfered with the binding of dopamine and prevented activation of the neuron. The scientists can study this because the have some special flouresent antibodies that bind with D2 receptors and they can "see" how much of the flourescent antibodies bind. When the patient's got a lot of 24.3.1 or other anti-D2 or anti-D1, it prevents the binding (messaging) by dopamine. Again the anti-D1 and anti-D2 are not binding with dopamine directly, but rather to the receptors to dopamine. If you know what a feedback cycle is, the anti-D1 and anti-D2 are acting as a random error signal in a feedback path making it so it's hard to "control" the signal. Buster

The research by Kirvan and Cunninham is indicating that it isn't too much or too little dopamine, but rather that the antibodies interfere with dopamine receptors preventing the regulation of signal. The analogy I use is that PANDAS antibodies are like loud commercials on a television that cause you to go over and turn down the volume and then when your regular show comes on you have to go back and turn back up the volume. This inability to control the "volume" because of the interference of the antibodies is what is causing the signalling issues/cross-talk. So it isn't the dopamine per se but rather that the antibodies are binding to the dopamine receptors and interferring that's causing the issue for PANDAS kids -- at least that's the theory.

Great news! Welcome back and glad to hear your news -- interesting about the eye blinking and glad to hear that has also resolved. Yeah!

Could be -- is your son already on azith? 0.76 U/L or less: Negative - No clinically significant amount of M. pneumoniae IgM antibody detected. 0.77-0.95 U/L: Low Positive - M. pneumoniae-specific IgM presumptively detected. Collection of a follow-up sample in one to two weeks is recommended to assure reactivity. 0.96 U/L or greater: Positive - Highly significant amount of M. pneumoniae-specific IgM antibody detected. However, low levels of IgM antibodies may occasionally persist for more than 12 months post-infection.

Well, the theory is that the endothelial cell is what is being "consumed" by the macrophage. So if you prevent any of the auto-antibodies from binding to the endothelial cell than then macrophage or APC can't present the antibody -- i.e., the macrophage can't consume the endothelial cell and present any antigen. Buster

Hi, Some things regarding working with Insurance. 1) Ask your doctor first whether they need your help. Sometimes they can work through the insurance claim items without getting the parents involved. 2) If the doctor has exhausted all options, call your insurance and ask to have a customer advovate assigned to your case. Get out of the claims space quickly 3) The next is subtle but important. If you work for a big company find out if the insurance is just the administrator of benefits or the provider of benefits. This matters. Many large companies are self-insured and therefore exempt from the equal protection for mental disorder -- but interestingly you can then work through your work to have the claim paid. 4) Once you get a client advocate, ask them if they are experienced in handling auto-immune disorders in children. Highlight that this is a child and with a distinct medical condition diagnosed by several doctors. If the person is not experienced in auto-immune, ask if they can help you navigate the insurance claim forms -- strangely enough asking for help is an incredibly effective technique. 5) If your child has recently been hospitalized, its often very helpful to explain to the advocate that you are asking them to advocate for your child and that you'd like to avoid additional hospitalization. You might then ask what documentation they rely on for determining treatment. 6) If they don't tell you, you might ask if you could provide them with peer reviewed articles indicating efficacy of treatment or whether that is better coming from your doctor -- there's all sorts of reasons to do this. Finally, ask if they can help explain whether they are denying your claim based on current research and if so can they provide a copy of the current research as it does not seem in keeping with the 2009 research that you and your doctor have discussed. 7) It will be extremely painful, but document everything. Every conversation, every mailing. While you will want to pick up the phone and call someone, it is actually better to use letters. You want to document, document, document. You must be persistant and patient. The easiest is to have your doctor help navigate on your behalf -- often a simple coding change can transition a denial to an approval. As painful as this sounds, remember to ask for help, as their advice on navigating the system, ask what they have seem where people have been successful. It is critical to recruit the advocate to your help. Regards, Buster

Actually no I meant that there are 42Million (going by 2000 census) -- although I see by the 2008 census that number has grown to 57M for the age group 5-13 http://www.census.gov/popest/states/asrh/t...-EST2008-01.xls Buster

I really like this article, what I got was the following: Auto-antibodies mark a cell for consumption by macrophages When a Macrophage consumes the cell, it keeps the tag of the auto-antibody The tagged macrophage runs into an appropriate T-cell and activates the T-cell The activated T-cell runs into a B-cell and causes production of more auto-antibodies And the cycle repeats (got to step 1) What's interesting with GABHS (and some other diseases) is that the exotoxins to strep can activate non-specific T-cells (i.e., that the T-cells get activated whether the specific antigen is present or not). Normally, this isn't a problem because the antibodies don't find anything to bind to and die off. However, if they are anti-host and find a binding site, then this can cause the feedback problem where the immune system goes nuts again. The paper then indicates that IVIG works by either: Saturating all the Fc receptors on the APCs so APC never presents the auto-antibody Binding to a suppressor mechanism (currently unknown) that prevents the APC from presenting any auto-antibodies Binding to Fc receptors on the endothelial cells so auto-antibodies have no place to attach and die (a) makes the most sense to me -- but who knows. Buster

Hi Athena, Extremely hard to say what is going on. It's possible the steroid burst had an effect -- it sounds like it was a single dosage but was likely quite a high dosage. Perhaps that was enough to prevent opening of the BBB or that you caught the strep so quickly after the 6th. Very hard to say. In our case, exacerbations were quite consistent with GABHS infections. Best regards, Buster

Not sure how to comment on your post. Are you saying you were back at baseline when you started the burst? Or that you are substantially better post Pred? Usually the burst is given during an exacerbation. Buster Well PANDAS is thought to be caused by 3 things: the creation of an anti-neuronal antibody (likely in response to GABHS) the failure of the immune system to recognize this as anti-host and suppress the antibody a breach of the blood brain barrier allowing the antineuronal antibody to reach neuronal tissue So while strep seems to cause #1 and the exotoxins of strep (and superantigens of strep) seem to cause the breach in #3. Many other things can cause or trigger a breach. Actually any inflammation (or even high blood pressure) can cause the breach. So if for some reason your child has high inflammation of the endothelial cells around the brain, then something other than GABHS could allow the existing antibodies (that live for 4-8 weeks) to interact with neuronal tissue. Thus while the non-GABHS might not be the "cause" of the anti-neuronal antibodies -- it can be the cause of the symptoms by opening the BBB. Buster

Well PANDAS is thought to be caused by 3 things: the creation of an anti-neuronal antibody (likely in response to GABHS) the failure of the immune system to recognize this as anti-host and suppress the antibody a breach of the blood brain barrier allowing the antineuronal antibody to reach neuronal tissue So while strep seems to cause #1 and the exotoxins of strep (and superantigens of strep) seem to cause the breach in #3. Many other things can cause or trigger a breach. Actually any inflammation (or even high blood pressure) can cause the breach. So if for some reason your child has high inflammation of the endothelial cells around the brain, then something other than GABHS could allow the existing antibodies (that live for 4-8 weeks) to interact with neuronal tissue. Thus while the non-GABHS might not be the "cause" of the anti-neuronal antibodies -- it can be the cause of the symptoms by opening the BBB. Buster

I haven't gotten around to posting all the papers, but here's a few articles: Psychosis in mycoplasma infection. http://pmj.bmj.com/content/65/760/96.abstract (1989) Mycoplasma pneumoniae Infection and Obsessive-Compulsive Disease: A Case Report http://jcn.sagepub.com/cgi/content/abstract/23/3/338 (2008) Abrupt-Onset Obsessive-Compulsive Disorder (OCD) in a Child With Crohn’s Disease http://psy.psychiatryonline.org/cgi/content/full/50/4/425 Antineuronal antibodies in a group of children with obsessive-compulsive disorder and Tourette syndrome. http://www.ncbi.nlm.nih.gov/pubmed/17113107 Neurologic manifestations of Mycoplasma pneumoniae infections: diverse spectrum of diseases. A report of six cases and review of the literature. http://www.ncbi.nlm.nih.gov/pubmed/10791130 Neurological deficit associated with Mycoplasma pneumoniae reversed by plasma exchange. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1546620/ Pathogenesis of neurologic manifestations of Mycoplasma pneumoniae infection http://www.biomedsearch.com/nih/Pathogenes...e/19664529.html 1981 Neurologic Disease Associated with Mycoplasma pneumoniae Pneumonitis Demonstration of Viable Mycoplasma pneumoniae in Cerebrospinal Fluid and Blood by Radioisotopic and Immunofluorescent Tissue Culture Techniques http://www.annals.org/content/94/1/15.extract Acute motor axonal neuropathy after Mycoplasma infection http://www.neurology.org/cgi/content/abstract/62/6/949 Neurologic complications of Mycoplasma pneumoniae infection http://www.medlink.com/medlinkcontent.asp I can try to sort through these and organize them. I haven't really pursued the Mycoplasma direction but there's lots of material on the topic.

Strangely enough she is in her late 30's/early 40's, but I think is just someone who works from experiences not from books or theories. She does okay when she can see someone with a broken leg or in a wheelchair or has a severe tic. It took me 4 meetings to realize I wasn't going to convince her with words and that to some degree it didn't matter. Buster

Actually, if you tended to get strep, you probably aren't a carrier. Usually a carrier is asymptomatic and does not have an immune reaction to strep. Also, ASO has to be taken within 4 weeks of a likely strep infection or it's value is not well understood. The fall rate of ASO is not studied. Buster

If you are curious about carrier state and what is measured by throat culture versus blood work: http://www.latitudes.org/forums/index.php?showtopic=5520 Buster

The principal at our school doesn't believe in PANDAS regardless of the amount of material we present to her. It hasn't mattered that we've got extraordinary documentation, diagnosis from a world-class psychiatrist, testing by the school psychologist, daily logs of handwriting changes, etc. At first I thought it was the principal just dealing with the reality of an underfunded school budget and not wanting us to use IEP resources for a kid who can't do math or spell but otherwise excels. Later we discovered it was more personal opinion -- she believed what she had experienced and thought it was just under-parenting or a defiant kid. Arggh, so incredibly annoying. After we had IVIG and our dd9 dramatically improved, the principal commented at the IEP meeting that the skill of the teachers had helped our daughter improve. Part of me was agreeing with her -- I'm glad for the great teachers, but another part was "you idiot, can't you see that her symptoms improved after we addressed the anti-neuronal antibodies." I don't think I'll ever convince her -- and I had to remind myself I didn't really have to -- it's just annoying. I'd think the school nurse should culture each kid that goes to the principal's office Buster

Chodnett, You should not be testing ASO or AntiDNAseB unless you need to confirm a strep infection that was 4 weeks or 6 weeeks earlier. Were results elevated? Did you have rising titers? You might find some answers here: http://www.latitudes.org/forums/index.php?showtopic=6266 Regards, Buster

In our case, we drew blood during exacerbation, then had throat and peri-rectal culture. She was positive on both grown cultures. We then did a second blood draw at 6 weeks post infection and both titers had actually dropped. This left us super puzzled. We ended up contacting multiple world-wide strep experts and asking them all sorts of questions like: if you don't clear a strep infection do the antibody levels drop over time? if ASO levels are dropping does that mean we missed the window? Can someone culture positive for strep and yet have falling titers? If culture positive at two locations how could ASO and Anti-DNAseB be negative? The best conclusion they had was that: a) our daughter might be an asymptomatic strep carrier -- but this didn't make sense as she had high fever at strep onset that strep was ping-ponging between children in the house or at school and so our daughter was clearing with ASO falling and then getting re-infected c) that there was a long term strep infection and that they've seen ASO and Anti-DNAse B eventually fail to rise to exhaustion of T-cells d) etc... Bottom line, they really didn't know. We are able to say that whenever our dd9 had an exacerbation -- her sister would be positive for strep so we think the ping-ponging makes the most sense. Buster

I totally agree. I started pulling stats for Autism, Bipolar, etc. I think the travesty here is how many kids end up on very significant psych meds which mask symptoms but don't address cause. I was very happy to see in the DSM-V that "tics due to a general medical condition" and "anxiety disorder due to a general medical condition" are both there. I was trying to figure out which medical condition would likely be used for coding. Seemed any of these are likely: 279.0 -- Deficiency of humoral immunity or 279.03 -- Congenital hypogammaglobulinemia or 279.10 -- Immunodeficiency with predominant t-cell defect unspecified or 279.4 -- Autoimmune disease not elsewhere classified or 323.4 -- Other encephalitis due to infection classified elsewhere or 323.62 -- Other postinfectious encephalitis and encephalomyelitis and then finish with either: 041.00 -- Streptococcus infection in conditions classified elsewhere and of unspecified site streptococcus unspecified I also agree the the direct cause should be investigated before just treating symptoms. Sort of before prescribing pain meds for "chest hurts" perhaps look for the sword sticking out or the signs of a heart attack -- likely treated differently Buster

I was wondering if anyone has run across any sampling data to indicate how many kids might have PANDAS or PITAND. Trying to triangulate the number, I started with population of children in US Age 5-14 was around 42Million in the US OCD estimates for children are 1%-2.3% -- or approx 1M kids Tic estimates are about the same (1%-2%) so call this another 1M kids -- of course there's some overlap The episodic type of OCD with minimal/no symptoms in remission is estimated by DSM-IV-TR at 5% -- so around 100,000 kids Swedo indicates that perhaps as high as 25% of OCD is PANDAS -- makes the average 100,000-250,000 Buster P.S. I added final bullet in edit after peglem's post... Also others highlight that we probably are way underestimating because of the number mislabeled with Autism, or Defiance disorder, or ADD, or ...

Yes, we had our first significant flair after a tooth extraction when our daughter was 7.5. We thought it could have been B12 deficiency (from nitrous oxide), but we ruled that out. What we think happened was that bacteria colonized in her throat was given immediate pathway to the blood stream. Buster

Hi WorriedMommy, Some of the antibiotics (notably macrolides) are anti-inflammatory and immuno-modulating. PANDAS is thought to be caused by 3 things: a genetic predisposition to creating an antibody targeting neuronal cells in response to GABHS infection a failure of the immune system to suppress the anti-host antibody a breech of the blood-brain barrier that allows the antibody to reach neuronal tissue In the case of azithromycin, it appears to shift the Th2->Th1 (extracellular response to intracellular response). In addition, the anti-inflammatory effect may help the BBB (#3). Finally, antibiotics may help reduce the severity of an infection by limiting the rate of spread of an infection -- i.e., it won't stop an infection but can slow it down so the immune system produces fewer anibodies. Titers are largely meaningless. I know doctors like to put more faith in blood tests, but in reality, unless you get the draw at a very specific intervale, the blood test doesn't tell you anything. Titers can confirm a previous strep infection but can't rule it out. A rising titer indicates that there was a strep infection sometime in the last 4 weeks (ASO) or last 6-8 weeks(AntiDNAse . The rate of fall of titers isn't known or studied. A constant titer is similarly without meaning. An elevated titer is sometimes treated as a rising titer, but actually most people don't know. This lack of tight correlation/repeatability of titers with symptoms in some children is what causes some doctors (such as Kurlan) to question the PANDAS findings (particularly the "AS" portion). Swedo, in her studies, selected children who did have such an association so that she could show the repeatable laboratory tests matching clinical symptoms and better isolate what was going on (i.e., the isolation of antibody 24.3.1 and the interference with the dopamine d2 receptor). There's more in the FAQ around titers http://www.latitudes.org/forums/index.php?showtopic=6266 We can extend the FAQ if you have other questions. Buster

The blood brain barrier is a set of cells around the brain that prevent proteins and other large molecules in circulating blood from getting into the central spinal fluid. Diseases like Multiple Sclerosis are disorders where the blood brain barrier is open and proteins can interact with the brain. A sort of fun site on BBB is http://faculty.washington.edu/chudler/bbb.html I tend not to use the words "atttack the basal ganglia" and instead use "interfere with the basal ganglia" because there isn't strong evidence that the basal ganglia is actually damaged -- but yes. What Kirvan and Cunningham found was anti-neuronal antibodies in the Central Spinal Fluid of kids with PANDAS (or with Sydenham Chorea) and this auto-antibody seems to have come from circulating blood. For this to happen, the antibody must cross the BBB. Ths can occur due to high blood pressure, significant stress, or inflammation (http://www.latitudes.org/forums/index.php?showtopic=6063&hl=T-cell). Well, sort of. If you see significant improvement in behavior then it is likely that your child's behavior is related to inflammation or is having an auto-immune response. So presuming you have the "P", "N", "D" of PANDAS, Pred would help fill in the "A" (for auto-immune). The "Associated with Streptococuss" would come from either throat culture or blood work. The main reason for trying to figure out if it's GABHS or something else is to know how to treat the condition (i.e., now that you know it is auto-immune and presents as a neuropsychiatric disorder -- what are the triggers). Buster

I was sitting in Barnes and Nobel and picked up a copy of DSM-IV-TR I found: 293.84 -- Anxiety Disorder due to a General Medical Condition This was surprisingly close:"The essential feature of Anxiety Disorder due to a general medical condition is clinically significant anxiety that is judged to be due to the direct physiological effects of a general medical condition. Symptoms can include prominent, generalized anxiety symptoms, Panic Attacks, or obsessions or compulsions (criterion A). There must be evidence from the history, physical examination, or laboratory findings that the disturbance is the direct physiological consequence of a general medical condition (Criterion . ..." "Although there are no infallible guidelines for determining whether the relationship between the anxiety symptoms and the general medical condition is etiological, several considerations provide some guidance in this area. One consideration is the presence of a temporal association between the onset, exacerbation, or remission of the general medical condition and the anxiety symptoms. A second consideration is the presence or features that are atypical of a primary Anxiety Disorder (e.g., atypical age at onset or course, or absence of family history)...." Similarly, within the 300.3 OCD, the DSM-IV-TR has under prevalence of OCD: "Community studies of children and adolescents have estimates a lifetime prevalence of 1%-2.3% and a 1-year prevalence of 0.7%. Research indicates that prevalence rates of Obsessive-Compulsive Disorder are similar in many different cultures around the world." Then later under course: "Modal age at onset is earlier in males than in females: between 6 and 15 years for males and between age 20 and 29 years for females. For the most part, onset is gradual, but acute onset has been noted in some cases. The majority of individuals have a chronic waxing and waning course, with exacerbation of symptoms that may be related to stress. About 15% show progressive deterioration in occupational and social functioning. About 5% have an episodic course with minimal or no symptoms between episodes." There are no references provided in the sections so it isn't know which studies are being referenced for the above position -- but this is what the doctor/psychiatrist/... is reading. I loved the next section Differential Diagnosis : "Obsessive-Compulsive Disorder must be distinguished from Anxiety Disorder Due to a General Medical Condition..." There's more but it made me think there was room within the DSM-IV-TR for PANDAS under the 293.84 coding. Buster