kimballot

Thank you so much for this article. It was very good but... unfortunately, leaves me with the impression that: 1. My son (who started on antibiotics at 4 months of age and has been on them most of his life) had a complete upset of his microbiome early on. 2. Replacing the lost bacteria is a great idea, but we have no idea exactly what type of bacteria needs to be replaced nor in what amount. 3. The effects of antibiotics are systemic, but bacteria replacement through oral probiotics will likely not replace the bacteria in, say, his ears or sinuses (though the comment in the article about transferring ear wax from the non-infected ear to the infected ear is very intresting!). 4. Mulitple strains of probiotics are not necessarily better than singe strains, since we have no idea what is missing and we don't know if the multiple strains work in concert or if they could have some sort of negative interactive effect. Now - I recognize that the article was fairly conservative as it was written in the New Yorker, so I am sure they would not go out on a limb to promote anything that could not be backed up 100% by evidence. So, my question is... given the scientific evidence we have now... what is the best thing I can do for my immune-deficient, PANDAS-prone 15 year old son probiotically, as he is on 3 antibiotics now and may very well be on at least one antibiotic for the rest of his life. He does take probiotics, but I feel like I am guessing at this more than anything. Thanks so much for your insights - I really enjoy your posts.

Yes - you can "upset the applecart" in different areas. For example, one theory of schizophrenia that is due to too much dopamine in the limbic system... so they give the individual meds to block dopamine, which does reduce hallucinations. The meds are better now, but the older dopamine blockers often produced some parkinson symptoms early on due to decreasing dopamine in the basal ganglia. Additionally the brain has plasticity and changes over time. The number of receptors actually change over time. So, people with schizophrenia who are on dopamine blockers for a long period of time actually can develop MORE dopamine receptors to try to accommodate for this. As they develop more dopamine receptors in the basal ganglia, they can start having unusual muscle movements called tardive dyskinesia. I believe this is seen less often now than in the past as I think newer drugs are better and controlling for this. However, that is why we need to be carful with meds that mess with these levels. It is not as simple as it looks on the surface.

My son has a long history of chronic sinusitis - no strep throat on culture. At age 7 we stopped all antibiotics as nothing seemed to help and we were just trying to figure out what to do. When we stopped them his tonsils turned completely white. ENT said "bingo" he must have been harboring bacteria in his yucky, large, cryptic tonsils all these years and whenever he went off antibiotics the bacteria went up to his sinuses and made us think it was another sinus infection. We had them removed and it was the best decision for him. He had 5 years of minimal pandas symptoms, decent health and "typical" development - until he was hit with some major infections at age 12. In hindsight, he also had common variable immune deficiency, but we did not know to keep an eye out for that.

I remembered someone else noticed this a couple of years ago and I found this thread http://www.latitudes.org/forums/index.php?showtopic=7632&st=0&p=62077&hl=bloodletting&fromsearch=1entry62077 that you might find interesting! You are not the only one who has seen this!

Yes -I absolutely agree. Cam Kinase is a precurser to dopamine. That is, one of the many functions of Cam Kinase is to produce dopamine.... so really, it may be just one more way that dopamine levels are being changed in our kid's systems - presumably by increasing dopamine. The idea behind Cunningham's work, I believe, is that the antibodies from our kids blood react with neuronal cells to produce cam kinase at higher levels than kids without PANDAS.... our kids' antibodies actually produce more Cam Kinase than kids with ADHD, OCD, or tics who do not have PANDAS symptoms (sudden onset associated with an infection). BUT our kids' antibodies produce less cam kinase than kids with sydenham's chorea.

I am wondering - did they put hte VERY LOW and VERY HIGH on the report? Those look like low end of normal and high end of normal ranges to me. I don't have my DS's ranges in front of me, but i know that one's he was high in ... he was over the upper limit. Also - as per the explanation I just wrote for LLMs question regarding the areas of the brain - it would make sense that your DS 13 had OCD and movement disorders as D2 receptors are found in high concentrations in the basal ganglia, which controls movement, while your DS11 had symptoms more closely associated with limbic system and cortex issues (D1 receptor). Your DS 10 is harder to relate to the ranges ... and I don't really have an explanation for that right now. again - I think this is all more hypothesis than fact at this time... I've not seen a paper or presentation about this. Perhaps others have?

So...if the receptor is blocked because an auto-antibody has shoved its way into the receptor, it prevents that receptor from re-uptaking the dopamine puddled up in the cleft. Does this cause neuronal signalling from the blocked receptor (I'll call him Al)? Al says "Hey Bob, send more dopamine - I'm not getting enough!" So Bob, the sending dendrite, sends more dopamine. The cleft puddle gets bigger. (thus, too much dopamine). But...Al still shows symptoms of too little dopamine. He's not getting what Bob is sending. Can you then have too much dopamine outside the neuron and too little inside? It would then become a balance problem (within vs. outside of the neuron) rather than too little or too much in the overall system? Because as Jill said, I swear my son looks like too little dopamine. (FWIW - neither of his D measurements were out of range yet he ticced severely). The attention deficits clearly get in the way of academics, even when in remission. And then I have the question of the state of affairs when not in a flare. As Jill asked earlier, can you have a general state of low dopamine when in remission that would benefit from tyrosine or amatadine or something that boosts dopamine re-uptake? Not exactly - From my understanding, if an antibody binds with the receptor it does not necessarily block the receptor. The antibody could act as an agonist and actually turn the receptor on... in that case it is mimicking the neurotransmitter. If it is binding with a neuron that produces Cam Kinase, it will produce more Cam Kinase.. which does many things, including help to manufacture dopamine. If the antibody is binding with a dopamine receptor and is acting as an agonist it is turning on the dopamine receptor. The neuron thinks it is getting dopamine and will act as if it had dopamine. The neuron will then do whatever it is designed to do when it receives dopamine.. and that depends on where the neuron is located. That is why changes in dopamine levels in the basal ganglia look different from changes in the dopamine levels in the frontal lobe or the limbic system. D1 receptors and D2 receptors tend to be located in different parts of the brain. This may help http://www.livestrong.com/article/141471-5-types-dopamine-receptors/ . So.. the problem, I think, is more WHERE the antibodies are attacking the brain - more than whether the dopamine is going up or down. I think that is why some of us see more emotional changes (limibic / D1), some see more ADHD symptoms (cortex / D1) and some see more movement (Basal ganglia / D2), and some times we get real lucky (sarcasm) and see it all. We also have to remember that all of this is theory right now. They are learning from our kids. In reality, this is probably a very simplistic model and is only a piece of what is going on. Many people think that cytokines and other immune responses also play a huge role in what is happening with our kids - hence the relationship to inflammation. Also, just because your child's antibodies tended to "turn on" D1, D2, or cam kinase, does not mean that those antibodies are currently in your child's brain. Antibodies are not supposed to be in brains. They cross the blood-brain barrier with infection or inflammation. It just means that if they did cross, then your child has more of a likelihood that this binding would occur than some child without aoutoimmune tendencies.

Ok- I have not had a chance to pull out DS's levels, but I will comment on this statement and couple of other statements made. My understanding of the Cunningham test is that they take serum from our kid's blood - the part of the blood with the antibodies - and then put it in a little dish (or tube or something) with some type of neuronal tissue and see what happens. When they put it in with donor basal ganglia neuoroblastoma cells (that would be live cells that originated from someone's basal ganglia), they can measure how much Cam Kinase is produced. Cam Kinase is an enzyme that is used in many neurochemical procsses, one of which is the production of dopamine. Kids with PANDAS make more cam kinase than other kids, but kids with syenham's chorea make even more... so the idea is that Cam Kinase must be leading to increased dopamine, which must be leading to our kids' problems. Regarding the receptors - A neural synapse is the juncture between two neurons. Electrical impulses travel down the axon of one neuron and reach the juncture. The dendrite from the next neuron does not actually touch the axon from the first one. Instead... there is a cleft between the two In order for information to travel across it has to travel chemically. Different axons produce different neruotransmitters. When the electrical signal gets to the end of the axon, the neurotransmitter is released into the cleft. The neurotransmitter travels across the cleft and binds to receptors in the dendrite of the next neuron. The fit sort of lock and key in that certain neurotransmitters will bind with certain receptors. Once the receptor receives information, it will send a signal to turn the next neuon on. When enough signals are sent, the neuron will turn on and send an action potential down the axon to the next synapse... and so on and so on. So... The problem with D1 and D2 receptors is that it seems that the antibodies in our kid's blood serum is locking into these receptors. So.. the the quote from the letter "Antibodies may induce increased signaling of neuronal cells and cause release of too much dopamine in the brain." indicates that we may have too much dopamine as a result of all of this. I hope that makes sense and is not more confusing!

Mustang Carole - Nice to see you on here again! Anyone in Nebraska area that could reach out to this family? It is hard to believe they've not consedered PANS given the how long they have been battling this... but you never know.

Hi - Lots of interesting posts recently about probiotics and gut health, and, with the help of some posts from ThinkGutBacteria and others, I am moving toward learning more about gut health and probiotics. I am sure that my ds15's gut health is a huge part of his condition. He started on antibiotics at 4 months of age and was not able to come off until age 7 - and that entire time we never even considered using a probiotic. I am sure that only added to his already depleted immune system and I KNOW he had major yeast problems. Around age 7 we learned about leaky gut, the "yeast connection" and fungal sinusitis and realized (somewhat) what we had been doing, and then spent the next few years avoiding antibiotics at all costs and promoting gut health - only to get hit with simultaneous H1N1, sinus cyst, and bartonella 3 years ago, and we are working now on recovery from that. He currently is on a gluten-free / dairy-free diet and we use Sacchyromyces twide daily. I throw in some acidophilus when I can but, honestly, do not do that regularly because I have a hard time remembering to give it to him 2 hours before/after ABX. I can give sacchy at the same time, so we just go with that. He is not on an antifungal at the present time, and I wonder if that is a mistake. So - I am wondering if there are some good gut- health sites or references that folks would recommend to help me to understand this better. Thanks so much!

I am only able to view the first minute and 51 seconds here. Not sure how to get to the rest of the chapters. Looks very interesting. Thanks.

Well.. welcome to the forum! It sounds like your son has had a plethora of diagnoses/labels, which is the experience of many parents here. There are certainly many biomedical things that can be happening with him which may or may not be PANS. You say that his first tic exacerbation began a week after fifths disease - and that was just last September. So he had sensory sensitivity, OCD and rages from a young age - but tics are a recent addition? Have the tics gone away, gotten worse, or gotten better since the September onset? My son has had PANS symptoms since toddlerhood, but they were always clearly associated with sinus infections and would go away when he started antibiotics. However, he was 12 years old before we really pursued the PANS (PITAND) track. At that time I went back and got all of his notes from ENT and from his pediatrician. I also dug out whatever I could find from preschool and from the school regarding behavior and grades, and made notes to myself about his behavior at holidays each year (ex: Hit cousin at his 4th birthday and had to leave early). The correlation between his illnesses and his behaviors was quite clear, as was the fact that he was ill much more frequently than most kids. In our case, this helped us to look more closely at his immune system. So -you might want to start with a list of all of his known illnesses and then look at your visits and phone calls to docs for his behavior and see if there is a correlation. Just one thought - I am sure others will have other good ideas for you.

What?! Are we reading the same studies? What are your references for "Probiotics for yeast will really only help the gut - they don't get into the blood and travel to the nose"? Many results show certain strains of probiotics and prebiotics helping in every corner of the body, so to speak, including nasal allergies, lung infections, skin eczema, brain hormone imbalances, blood pressure, you name it. For this particular question, I'd look into alternate causes of stuffy noses like non-allergic rhinitis and laryngeal reflux. Wow - not that I've seen or am aware of, so please post. I am 100% for probiotics and use them regularly but I was under the impression that probiotics do little for sinus fungus directly. I certainly understand indirect benefits in reducing gut inflammation, leaky gut, and reducing nasty stuff being spilled into the bloodstream.... but I was not aware that oral probiotics repopulated sinuses. I would love to see some studies. You can post here or pm me if you'd like. Thanks!

I hope you are one of the true success stories - one exacerbation caught early and properly treated. That would be great!!! That is what I hope for for all of our kids one day!

Well.. no sinus infection is good news! Was the CT scan read by a radiologist? You should get the report. Sometimes they can see mucosal lining thickening consistent with allergy. Also, you can have a stuffy nose without having a sinus infection - that is what happens when most people get a cold or have nasal allergies. The question is why this happens with antibiotics. Is she having an allergic reaction to the antibiotics? Are the antibiotics increasing the fungus in her nasal passages? Lots of questions. Perhaps your ENT can help. Probiotics for yeast will really only help the gut - they don't get into the blood and travel to the nose. Antifungal meds or an antifungal nasal rinse are probably your best bet, but I think you said before that she was on an antifungal - correct?

sorry - I did not read your initial post thoroughly enough! Is your son still on antibiotics? It is possible that his initial reaction was to mycoplasma and / or strep... hard to know which or if it was both, I would think.. No subsequent exacerbations with strep exposure... great! Not everyone has an exacerbation with exposure. It does not mean that the initial trigger was mycoplasma.

Yes - your child can have an exacerbation with ANY infection... which would be considered PITAND or PANS - not specifically PANDAS. Mycoplasma is a common problem. I don't know about "typical" kids, but kids on this forum have had mycoplasma more than once.

That is a great find (in a twisted sort of way).... I am sure they will culture it when it is removed to make sure it is just fungal and also to see if it blocked up the sinus and has bacteria growing behind it. Did the radiology report identify the mycetoma - or did the ENT just figure it out? Good for you for pursuing this!

I am sure folks on the lyme forum could answer this with great detail. My son was also low. He was 15 at the time of the blood draw. I was told that CD 57 is questionable in children, and is much more valid in adults. In our case, it was just one of several indicators of lyme/bart.

I am a strong believer in gut-belief, but I also know that lyme and bart are tricky and are not always as they appear. My son has bart and it is bear to fight. Sometimes he seems worse when we start new ABX - but it is because the ABX are really fighting the darn thing. I find a lot of ideas from the lyme forum here too. I really wonder about immune deficiency with your child.

I am so sorry. I did not realize that you've been seeing Dr. J for 2 years!. Now I understand why you are thinking it might be fungus and why you are targeting sinuses. You are in a difficult situation because it is hard to tell if the worsening with ABX is due to increased fungus or due to herxing because the ABX work. Please keep us posted on thesinus CT scan. Hoping you get some answers soon!

PANDAS diagnosis aside..... isn't your child the one who has had increased stuffiness with antibiotics? Isn't your child the one with congestion? ENT saw nothing? I can understand not wanting to do a sinus CT scan if there are no signs or symptoms of sinusitis, but your child has had symptoms. It will be interesting to see what comes out in the CT scan. Also, you say that you need to find out where the infection is... but I thought your child had lyme and/or bartonella. If so, that IS an infection that can trigger a PANDAS reaction... plus lyme and bart themselves have symptoms that are similar to PANDAS. So, I don't think your child has to have yet another infection. I also saw in another post that your child has elevated mycoplasma levels. That is the bacteria that causes walking pneumonia. It is also frequently transmitted with ticks if someone is bitten. Mycoplasma can also be the infection that triggers PANS. So, I think it is wise that you are getting the sinuses checked out, especially with the stuffiness, but don't be surprised if they turn out to be fine. Your child has plenty of other "things" messing with her immune system to cause the reactions you are seeing. If you are seeing Dr. B your child will likely be tested for immune deficiency. Given the plethora of infections she seems to have and the history I've been reading, she may have common variable immune deficiency. It will be interesting to see if that turns out to be the case. If it does, it will help to explain a lot.

Pictures are the best thing... sometimes we don't really understand something until we view it in hindsight. Keep us posted! Good luck!

I am wondering if a doc has seen your son for the ringworm dx. I am asking because when DS15 was 10 he had something on his torso that I described to the doctors office over the phone and they told me it must be ringworm as we had just come back from vacation and he had spent some time in the public pool "spa" (Obviously - we had no clue about immune deficiency or PANS then!). Anyway, the rash was round and on his trunk. We treated with lotrimin and it went away, so I assumed ringworm. As I look back over bloodwork, it was around that time that he started having more flares and shortly after that started showing low antibodies and positive titers for mycop. In retrospect I wonder if he wasn't bitten by something at that time. We now know that he has bartonella and has had it for a long time. Anyway - my point is that I wish I had brought him in to have the rash looked at and (at least) I wish I would have taken pictures of the rash so I could look back and show it to experts today.

As I was reading your post I was also thinking of lyme and was glad to see that you have also been entertaining that notion. Also, when you say there was a worsening with steroids - how long were the steroids given? My son always did worse the first week of steroids as they were building... but then did better in the end. Of course, if your child does have lyme or an ongoing infection then steroids are not the best idea because they suppress the immune system. Has your son had a good immune workup for immune deficiency, also. Common variable immune deficiency is frequently an underlying cause in these kids with repeated infections.... and most of the time the low antibodies do not show up in early childhood. The immune deficiency foundation says many people are not diagnosed until adulthood, even thought they have repeated infections. If he has some type of immune deficiency it could really underly a chronic infection that is resulting in enlarged spleen. Regarding clonodine - many kids with tourette opt to NOT use meds for tics becuase they either don't help or have bad side effects. I don't think that is uncommon from what I hear. You are saying that your son is not that bad, but really it sounds like you have a lot on your plate and are working hard to sort through it all. I wish you the very best!