jan251

She is very young; you have time. Many of us undergo a mourning process when we reach that lonely place where we realize that the mainstream, inside-the-box medicine can't help our kids. Have you made an appt with a PANDAS specialist yet? I know the waiting is hard. Be thankful that she is not school-age yet. Be patient with yourself - you will need strength for the journey to get to the bottom of this.

The sudden onset and the urinary issues would be relatively specific to PANS, if I recall correctly. However, personally, I don't like the boxes we have in medicine. Looking at the big picture, it is obvious that the infection had something to do with the symptoms you saw. The connection is probably the immune system, i.e. inflammation, probably of a specific type. Immune and nervous systems are connected. Especially considering the history of lyme, I'd wonder about the status of the immune system in general (blood tests) and whether the viral and lyme infections (and lyme co-infections) are still lingering (more blood tests). Whether to take a more immune system approach or an approach that focuses on the infections is impossible to say - there seems to be some disagreement on that among PANS/PANDAS docs - maybe both is the answer. The onion has several layers and there is no one route to wellness. I'd probably start with a PANS/PANDAS doc though many are not as experienced with lyme - it just depends. Maybe set up appointments with both a PANS/PANDAS doc and a lyme doc.

For what it's worth, I happened to read an article today about a child who had Sjogren's antibodies though I'm not sure how that was related to her case - she had autoimmune encephalitis. Maybe it's just another indication to look in an immune system direction...

I don't remember seeing this June 2016 study posted - my apologies if I missed it: PANDAS: Baseline Immunoglobulin Levels Predict Achievement of Remission at One Year Following IVIg Therapy

Just wondering - have you ever compared Enhansa to other versions of curcumin? I buy the Meriva version by Jarrow, mostly for myself, for random things - I think it's the cheapest Meriva available. It hasn't done much for my child but doesn't seem to hurt either, and it's been so long since I've given it consistently, I wonder if that's another thing I might throw into the pot... (I might even have some Enhansa around here somewhere, though they're the tiny capsules. We did the powder version before he was swallowing pills, and never got anywhere aside from making messes, though again dose is a question.)

So the OCD and tics left with antibiotics, but loss of language, loss of motor skills, and anxiety remain. If it were me, I'd still be blaming PANS/PANDAS here and assuming this is not permanent, but treatment may not be straightforward or quick. We've been working on this for two years now. Funny thing is that before PANDAS, my child had developmental delays, low levels of sensory stuff going on, speech and language issues, etc., but it wasn't until PANDAS that there were relatively short moments of overwhelming anxiety where he really "looked" autistic, even to the professional we saw for CBT. In those moments, it's downright disturbing for me to try to look at him as an unfamiliar observer rather than the mom who knows exactly where he's at underneath the compulsions or whatever. For us, there are layers to the puzzle, and antibiotics provided very little in the way of symptom relief. We're working on IVIg and if we get improvement, at some point hopefully we'll be in a place where trial and error with methylation, etc. will help us do the fine-tuning I expect will be necessary. Good luck with the PANDAS doc. I know the waiting is hard.

I don't think anyone knows the answer to this question, but I'd be inclined to think that a rapid regression into autistic symptoms may well be a PANS/PANDAS exacerbation. That would make much more sense to me than permanent damage. (thinking for a moment, what would we even mean by permanent damage? Nerves that couldn't be regenerated? Antibodies or infections blocking other molecules from attaching as in molecular mimicry, but permanently? Or something like levels of neurotransmitters?)

We haven't yet found a path to healing for our child, so my thoughts aren't worth much. Igenex is considered much more reliable for lyme, though I'm still not sure what to think myself. Our insurance did not cover the Igenex test. Our ds got worse with certain antibiotics (such as minocycline) that ought to be good for lyme; perhaps our ds does have lyme, but the treatment path is daunting even though we have done months of antibiotics and herbal treatments to no effect. I don't know anything about Sjorgen AB, though isn't that an autoimmune issue or is it an infection? I would not assume that high strep antibodies and OCD are independent even though there isn't always an exact correlation between symptoms and rise/fall of antibodies. I'd take the high strep antibodies as evidence that there might still be ongoing strep lurking, and ongoing strep could, in turn, contribute to the OCD. I'd ask the doctor about trying different antibiotics (e.g. zithromax, omnicef, etc.) to try to find one that didn't make him worse and yet might still address strep. Making the OCD worse beyond a few days is not a viable treatment path, at least in our house, as it's difficult enough to tolerate the OCD even when it isn't "worse." On non-response to prednisone vs trying IVIg, I can't say. Our ds did not respond to prednisone - all it did was make him cranky - and yet after over a year without relief, we reached a point in the road where we were ready to try IVIg. We are praying and keeping our fingers crossed that this will produce results. What I feel confused about is whether we will need to add more antibiotics to kill off infections (strep, mycoplasma, lyme) once the immune system is working better. Generally, I might assume that OCD worsening with antibiotics and prednisone is a sign that there is some type of infection, or multiple infections, present. How to go about treating is another question, but I'd keep trying.

My two cents on a couple of possible angles to consider: (1) lyme - was the test through Igenex or a regular lab? (2) immune system issue. If there hasn't been testing of the immune system - IgG levels and so forth - I'd look at that next. As much as antibiotics are a first-line treatment, there really is no agreed-upon, conventional treatment for PANDAS. Besides antibiotics, IVIg has also been studied. My guess is that many people may need a multi-faceted approach to treatment. If strep is still around, I'd want to be on some antibiotic if possible, for a lengthy duration. It would not be unusual to need to try a few different antibiotics before finding one that at least didn't hurt even if it didn't clearly improve the ocd. FWIW, my child tends to respond similarly - either the same or worse on antibiotics and worse with steroids. He had a positive lyme test through Igenex but negative through Labcorp. Unfortunately, treating lyme and confections led to no improvement. We are now working on IVIg for an immune deficiency. We don't know yet whether we'll have to return to lyme treatment after IVIg (eh, I often do some herbal treatments on the side, but no major antibiotics at this time).

One of my kids had strep as a baby - which isn't supposed to happen - and the ped swabbed the rear end (based on symptom of mucus in diaper). But we never swabbed panda kiddo's rear end. For what it's worth, sacchromyces boulardii is the one probiotic that is horrible for my ds, though I'm sure others here have had better luck with it. It just did something too upsetting to the microbiome for him and the ocd onset was potentially related to when I started giving it to him. It was really weird and I never quite figured out that angle.

How lame that they told you "just a bacteria." I assumed it would be e. coli because that's the most common cause of UTIs, and accordingly, would be what the culture was testing for. That doesn't mean there aren't other types of infections, of course. For a UTI, I'd strongly consider adding D-mannose (comes in tasteless/sweet powder or capsules). Is treating the UTI the only purpose of the current antibiotics? I suppose it's possible for that infection to be the primary problem but I might wonder what else is going on that could be causing PANDAS symptoms. Have you done strep titers? Some kids can also be sensitive to the type of probiotic. What are you using - maybe switch it up?

I can't answer your question about the antibiotics, but I would generally tend to blame the immune system, especially when there are things like bruising going on. When you go to the doc, have a CBC included in the bloodwork to check platelet levels. Though come to think of it, if you are doing a lot of motrin, maybe that's the cause. Gut health is still a big mystery for me and it is part of my kiddo's pans/pandas. We had a problem with s. boulardii (as in florastor, though we were using a different brand), for example - it immediately, like within hours, exacerbates ocd for my ds. For the UTI, a positive test usually indicates e coli, yes? I would add in D-mannose, which can be very effective. Vitamins are such an individual thing (for example, we now think that my dd, who has a bunch of genetic mutations and polymorphisms such as compound heterozygous for mthfr, needs to avoid folic acid, which is in many multivitamins not to mention food). Good luck with the doc - I hope next week gets here soon!

This is a very old thread but...has anyone tried pterostilbene for purposes of a natural anti-inflammatory and did you find it helpful? I'm always on the lookout for additional natural anti-inflammatory options to add to our collection. We have resveratrol (japanese knotweed/polygonum cuspidatum from Seeking Health) and curcumin (Meriva from Jarrow). Pterostilbene has been studied for a variety of issues in addition to cancer. I noticed this study on mice and anxiety: Anxiolytic action of pterostilbene: involvement of hippocampal ERK phosphorylation. Pterostilbene attenuates lipopolysaccharide-induced learning and memory impairment possibly via inhibiting microglia activation and protecting neuronal injury in mice. Pterostilbene exerts anti-neuroinflammatory effect on lipopolysaccharide-activated microglia via inhibition of MAPK signalling pathways

What helped my ds, not really for any reasons we can explain: - magnesium citrate (this comes either in capsules or in a powder - we used to mix the powder with water and sugar to make a "lemonade") - D-mannose - this should only have helped if there was ecoli in the bladder, so I'm not sure this makes sense, but it helped (also comes in a sweet/tasteless powder) - antibiotics

Bearmom, do you think this is the study you're asking about? https://clinicaltrials.gov/ct2/show/NCT01281969 No results posted. Data completed last Dec but the study will not be finished until Dec 2016. It's interesting to me that the PANDAS studies with IVIg are typically a one- or two- treatment deal, whereas in contrast, our doc is recommending a gradual dose ramp up and then every 3-4 wk at full dose to prevent IgG levels from going down. Perhaps that's because there's an immune deficiency in our case, but I wonder whether those patients for whom IVIg didn't work may have had a different experience with a more frequent dosing schedule of IVIg. So much is unknown! As indicated by the reference to immune status of OCD patients toward the end of that conference link, it would seem wise to include the immune parameters of PANDAS patients enrolled in IVIg studies. Who has an official deficiency, an unofficial deficiency, or no deficiency, and among them who responded to what dose of IVIg, would all seem to be incredibly pertinent information. Little studies that don't do this, and give IVIg once or twice seem like random shots in the dark with regard to the odds of benefit. And that doesn't even get into other possible parameters, such as infection titers and genetic defects affecting methylation and so forth. I suspect that it's hard to design such a study; I just hope that study results don't provide misleading information, where one method of dosing doesn't work for a subgroup whereas another method of dosing might, if it were studied.

Here is an article (now two years old) that lays out a basic testing roadmap and might be worth bringing to your doc. http://ndnr.com/autoimmuneallergy-medicine/elucidating-pandas/ In particular, I would consider adding testing for IgM/IgE/IgG total and IgG subclasses, a peek at immune system functioning.

I had not heard of this but I would be very skeptical. As the condition itself is very controversial, I don't see how it would be possible to know what genes makes one susceptible and what the point of knowing that would be. For genes, in my opinion, it would make more sense to run 23andme for $199. One can find out about methylation and detox genetic polymorphisms. Even with those, there isn't necessarily one clear path on how to address them, though I do think they can be informative. But $36,000? Absolutely no way would I do that unless there were a very clear treatment plan coming out of the results. I like to keep an open mind but it doesn't sound like the doc provided enough info.

Have you tried any natural anti-inflammatories, such as curcumin or resveratrol? (in my personal estimation, a capsule of Jarrow Meriva curcumin would probably be comparable to 200 mg ibuprofen in anti-inflammatory effect.) It sound like something is still wonky with the immune system and/or there is infection present if symptoms return when you don't give the ibuprofen.

I think Biaxin might have the same QT issue but I'm no expert; ask the doc. If you are interested in herbal treatments for myco, check out Buhner's book and also his website. The protocol in his book is different - I think the website is supposedly the most up to date but I found the book to be very informative.

For starters, has the immune system been looked at (for example, IgG subclasses) ? What infections were found in the tonsils? That would seem a good place to go, treat for those. Mycoplasma can be a long-term challenge to treat. Zith and Biaxin are among the usual choices. It is encouraging that Bactrim seemed to help though there are a number of things Bactrim may treat, such as bartonella, usually in combination with something else. Has prednisone helped before? It can be unhelpful in some cases such as with lyme and/or the usual coinfections, of which myco is one. Has he ever taken NAC? Might also be something to consider for myco. Good luck - that's a significant time crunch!

Thinking out loud, how might intestinal health, i.e. "the second brain," be involved in inflammatory processes involving lymph? Platelet interaction with lymphatics aggravates intestinal inflammation by suppressing lymphangiogenesis. http://www.ncbi.nlm.nih.gov/pubmed/27313177

I thought it might be interesting to see if there's anything new on this topic (original full text) New Brain Lymphatic Vessels Drain Old Concepts Aug 2015 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4563157/ Get It through Your Thick Head: Emerging Principles in Neuroimmunology and Neurovirology Redefine Central Nervous System “Immune Privilege” April 2016 http://pubs.acs.org/doi/abs/10.1021/acschemneuro.5b00336 Commentary: Structural and functional features of central nervous system lymphatic vessels James J. Bradstreet,1,2 Marco Ruggiero,3,* and Stefania Pacini4 Dec 2015 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4686591/ The meningeal lymphatic system: a route for HIV brain migration? June 2016 http://www.ncbi.nlm.nih.gov/pubmed/26572785

I believe the strep that impacts the mouth is not usually GAS. It is usually strep mutans. I do not know whether azith kills that - that would be something to look into. There is an herbal product that does kill strep mutans called flavescent sophora root (a.k.a. sophora flavescens, a.k.a. ku shen; FWIW, I have the one by Nature's Health. In our house, this product has been helpful for mouth germs.) Good luck with the extraction. We have not had a problem with braces causing a flare though ds has been in a two-year-long flare at this point, so who knows. He seemed to do very well back when he had his palate expander, which was removed a few months prior to PANS onset (hmmm...).

The first study cited in the article is very, very interesting and well worth a read for those who like to read medical studies. I don't recall seeing it before. Group A Streptococcus intranasal infection promotes CNS infiltration by streptococcal-specific Th17 cells Unfortunately, I find any discussions of BBB a bit confusing in light of the discovery of lymph vessels directly going to (exiting from?) the brain that was published last summer. I was sort of skimming but I didn't see that discovery noted in the study as a possible avenue for immune system components reaching the brain. I hope to read through this study again later, more carefully, for a better understanding. While Dan Shen (salvia miltiorhizza, as Buhner calls it if I recall correctly) closing the BBB is also an interesting idea, it would be helpful to know whether salvia has actually been used in any PANDAS patients in her experience or anyone else's experience, or whether the discussion is entirely theoretical. It seems to me that a lot of herbal treatments should be theoretically useful in PANDAS/PANS, especially for the underlying infections or for interrupting inflammatory processes, though we have not seen success, potentially due to the complexity of my child's case. (I do happen to have Dan Shen, the Planetary Herbals Salvia, in my cabinet though we did not use it for any significant length of time. If I were to try it again, I might rather buy the Nature's Health brand instead, which comes in a lower dose capsule, rather than the giant, hard horse-pill Planetary version that we have that I'd break in half or thirds or quarters and put inside an empty capsule.)

That's interesting! The discussion in this article conflates folic acid with folate when they are not processed the same by everyone. It all goes back to the methylation cycle. Multiple polymorphisms in various combinations may be helped by supplementing only some portions of the methyl cycle but not others. Many people with MTHFR do not process folic acid well and may be unable to convert it into folate. Others find difficulty in supplementing folate itself because other parts of the methyl cycle aren't working well due to genetic polymorphisms. It should not be surprising to the researchers that the one-size-fits-all approach of supplementing everyone via almost the entire wheat-related food supply (in addition to the standard prenatal vitamin recommendations) might result in unintended consequences. (Completely random thinking out loud without actually knowing the answer: do gluten-free food products contain supplemental folic acid? What if some people's benefit from GF isn't related to avoiding gluten but to avoiding folic acid?) Indeed.