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Psychiatrist on 'Psychlogy Today' website advocates Tonsillect


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Hi all,

 

I found these two articles on the 'Psychology Today' website by a psychiatrist out of California who treats PANDAS with tonsil/ adenoidectomy.

 

http://www.psychologytoday.com/blog/attention-please/201102/evil-pandas-scourge-the-brain

http://www.psychologytoday.com/blog/attention-please/201107/evil-pandas-part-ii-adult-affliction-treatment

 

My son still has a borderline high ASO titer now (200, with the lab in question considering >150 as elevated) after over two years on antibiotics. We did the Cunningham labs twice. Last time, a year ago his anti-neuronal antibodies had all come down to borderline high but his Cam Kinase II was still high at 167. Dr. Cunningham commented in her notes that to her those antibody levels were still high and still causing the elevated Cam Kinase. Since we can't get the Cunningham labs anymore, we are wondering if the ASO, which hasn't budged down at all in about two years indicates that his anti-neuronal antibodies are also still borderline high, since, if I understand it correctly, they are all antibodies to GABHS. At this point we are exploring removing my son's tonsils and adenoids in case they are a source of ongoing infection.

 

We corresponded with the psychiatrist and he believes that for the ASO to remain elevated, there must be a source of ongoing infection. Our local ENT agrees, so we may be headed down the T&A removal route, even though I know it is controversial.

 

Alex

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From what I understand....and I may be wrong....Cunningham's tests are NOT specific for strep. Antineuronal antibodies are antibodies to self-tissue, not strep. Right? Cam K is elevated from inflammation due to infection....again, trying to understand this myself.

 

What are your sons symptoms? Have they remained elevated (the symptoms) along with the high ASO? If symptoms are gone, who cares about ASO, in my opinion. Have you tried IVIG or steroids?? Who is your pandas doc?

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our dauhter had her adnoids removed in 1st grade. Her tonsils removed in 5th grade. She developed PANDAS in 6th grade. I also have read soem things on here that perhaps Tonsils help with the immune system. Don't knwo at all, the opinions oscillate by the day on what to do.

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Hey Alex,

 

Where have you been hiding??

 

How are ds's teeth? All perm teeth grown in?

 

Sorry this dance continues for your family. Just had an appt with new ped for both girls and it was unfortunately predictable. All I got out of it was scripts for both girl's swimmers ear. And lectures about vaccines and meningitis. Grrrr. Thank goodness I had a letter from Dr B for both girls. I love the way they taut their vaccination rate in the waiting room. Do they get some type of monetary bonus from insurance companies for high vaccine rates? I'm not a big conspiracy gal, but it sure has me wondering. Oh yeah, and he recommended therapy for all we've been through (sigh)

 

Missed you. Hope to see you around more.

 

Jill

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Alex-

 

Miss you too!

 

Hope things are ok.

 

Both of my kids had T&A.

 

The first one had them removed for sleep apnea, she had onset of pandas 2 years later.

 

The younger one had hers removed due to pandas. She relapsed 1 week post op :(

 

Both have had strep since T&A (older, twice- younger, once).

 

All of this being said- I would do it again. Both of their tonsils were extremely infected when removed, which the ENT's did not see prior to extraction. Also- my kids have relapsed and remitted, but we haven't (so far, fingers crossed) had very chronic states- if we did, I might be nervous there was some bacteria smoldering in infected tonsils.

 

I would do abx prior to, during (IV), and after surgery. I might ask the ENT about a course of clindamycin after surgery. I would also have your immunomodulating treatment of choice (steroids, ivig) on deck, if pandas increases.

 

As with everything with this disorder- go with your gut...

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For what is worth-- my now 6 yo ( who probably has PANDAS, also-- though I hate to say that yet) had a MASSIVE episode of paranoia and rage) the day after her tonsillectomy. She had adenoids out the year before. This was at age 3 1/2-- vocal tics started at 4 1/2, fears and sensory issues at 5 1/2 and it all continued until steroids in Feb this year- right before she turned 6.

So, I think the removal of her tonsils made an impact-- she went bonkers the say after-- but it remitted.

 

My older daughter has tonsils removed about 6 months post PANDAS onset- made no noticeable difference. Tonsils were tested for for multiple pathogens-- none found.

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Ugh. This scares me. We just decided to follow Dr. L's urging to remove tonsils. She was irritated that they didn't do it 2 years ago when they took her adenoids. Never had diagnosed strep (likely just missed it by not taking her in), until yesterday. And NO strep symptoms....just tics going from normal-all-day to nonstop for 10 days. Finally got first strep test. Who knows how long she'd been carrying it, etc. Now I'm worried it won't help/will make things worse.

 

our dauhter had her adnoids removed in 1st grade. Her tonsils removed in 5th grade. She developed PANDAS in 6th grade. I also have read soem things on here that perhaps Tonsils help with the immune system. Don't knwo at all, the opinions oscillate by the day on what to do.

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From what I understand....and I may be wrong....Cunningham's tests are NOT specific for strep. Antineuronal antibodies are antibodies to self-tissue, not strep. Right? Cam K is elevated from inflammation due to infection....again, trying to understand this myself.

 

What are your sons symptoms? Have they remained elevated (the symptoms) along with the high ASO? If symptoms are gone, who cares about ASO, in my opinion. Have you tried IVIG or steroids?? Who is your pandas doc?

 

Hi eljomom,

 

I just reread both the papers Dr. Cunningham sends out with the results of the labs. Definitely very challenging reads. Here are the links.

 

http://intramural.nimh.nih.gov/pdn/pubs/pub-15.pdf

http://intramural.nimh.nih.gov/pdn/pubs/pub-19.pdf

 

I could literally look up every third word for a definition. I did look up a lot though. The gist of the papers, as I understand it, is that GABHS, strep throat, has proteins on it's surface that are similar to proteins in the human body, in the heart, joints, brain, etc. The immune response to the infection produces antibodies which identify the strep throat bacteria by those proteins, but get confused by the similar proteins in the heart, joints, and brain and attach to those tissues as well, or instead. In Rheumatic Fever, this immune mistake results in the destruction of heart tissue or joint tissue. In Sydenham’s chorea and PANDAS, the result is non destructive, but the antibodies attach to brain tissue and cause excess production of a brain protein call Cam Kinase II.

 

Cam Kinase II plays an important role in brain signaling and excess amounts of it screw up the signaling which, as the hypothesis, or theory or whatever goes, causes Sydenham's chorea and PANDAS. So, in a nutshell antibodies to strep get confused, attack the brain, cause excess Cam Kinase II which negatively impacts brain signaling causing the movement and behavior disorders of Sydenham's chorea and PANDAS. So the papers are specifically talking about antibodies to strep throat, and it is not the infection that directly causes the brain problems, it is the antibodies the immune system produces to get the infection.

 

That's why the results from a plasma exchange can be so dramatic. The plasma contains the antibodies, if you exchange it for new plasma, you get rid of all the antibodies, including the bad ones.

 

I'm sure the above will be painful for Buster to read, if he does.

 

My son had Plasma Exchange and multiple high dose IVIG's and over two straight years of antibiotics, and unfortunately is still struggling. When he went in for Plasma Exchange, his ASO titer, another strep antibody, was 200. When he came out it was at 20(they don't completely exchange the plasma, just most of it). A few weeks later, I hate to say, when he relapsed, his ASO titer was back up to 200, where it has stayed for the last two years.

 

We can't get the Cunningham test now, but if the ASO titer won't go down, I am starting to realize that we don't have any reason to think that those other bad antibodies to strep will go down either. And if they won't come down, why not? The psychiatrist in the articles, and the ENT's he has trained would say it is because we have an ongoing battle with some sort of strep infection. In fact that is exactly what the psychiatrist said when he corresponded with us. Our local ENT says the same thing.

 

That's why I found those articles interesting and they are one of the reasons that in our particular case, we might give the tonsillectomy route a try even though I realize it doesn't work all the time or maybe even most of the time. We've got to do something.

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Hi all,

 

I found these two articles on the 'Psychology Today' website by a psychiatrist out of California who treats PANDAS with tonsil/ adenoidectomy.

 

http://www.psychologytoday.com/blog/attention-please/201102/evil-pandas-scourge-the-brain

http://www.psychologytoday.com/blog/attention-please/201107/evil-pandas-part-ii-adult-affliction-treatment

 

My son still has a borderline high ASO titer now (200, with the lab in question considering >150 as elevated) after over two years on antibiotics. We did the Cunningham labs twice. Last time, a year ago his anti-neuronal antibodies had all come down to borderline high but his Cam Kinase II was still high at 167. Dr. Cunningham commented in her notes that to her those antibody levels were still high and still causing the elevated Cam Kinase. Since we can't get the Cunningham labs anymore, we are wondering if the ASO, which hasn't budged down at all in about two years indicates that his anti-neuronal antibodies are also still borderline high, since, if I understand it correctly, they are all antibodies to GABHS. At this point we are exploring removing my son's tonsils and adenoids in case they are a source of ongoing infection.

 

We corresponded with the psychiatrist and he believes that for the ASO to remain elevated, there must be a source of ongoing infection. Our local ENT agrees, so we may be headed down the T&A removal route, even though I know it is controversial.

 

Alex

 

Alex - thank you for your excellent explanation of Cam Kinase and for these articles.

 

I agree that if strep titers are high there is likely an infection somewhere... But here is my question - how do you know it is tonsils? I want to say that I am not opposed to tonsillectomy when needed - it put my own son in remission for about 4 years and I wish we'd done it sooner.... but I think you really need to have some clue that the tonsils are a problem. Also, if my son were having ANY surgery again I would request that he be put on very strong antibiotics for several weeks beforehand to reduce the risk of strep or other antigens being introduced into the blood. In retrospect, I think my son's first exacerbation was triggered by adenoidectomy at 18 months of age.

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Hi Alex!

FWIW, my DS had a T&A 10 months into things, a month prior to Pex in '09. It helped him greatly. He hasn't had an issue with strep since. (of course, he's also been on a slew of abx and as you know, we now have the lyme battle going on, but no regrets on the T&A). With all you've been thru, I think you're right to give it a shot. It may not be "the" magic key, but I doubt it could hurt and the upside for your guy could be huge. Please keep us posted!

 

Laura

 

(BTW - Dr C has emailed a few members saying that she realizes lyme can cause elevated CamK. Certain M proteins on the outer surface of certain strains of GABHS are very similar to certain proteins/strains of borrelia. Kissing cousins. She published a paper about a decade ago on lyme autoimmunity tho her focus was on the heart. But similar theory. Your recap of her hypothesis is also my understanding, but my understanding is that she has come to say that CamK elevation isn't unique to strep. I believe more emphasis is put on her anti-neuronal measurements but my grasp of this has gotten rusty.)

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Alex---wow! That is exactly what I was thinking about this morning....the usual. Wake up. Sigh. STart thinking about pandas. Make breakfast. Think about pandas. Or pitand. or pans. or whatever the @#$& it is anymore. But what I was thinking is that I am a scientific person. I need the science behind it. So thank you for putting it in the beautiful nutshell.

 

LLM---I agree...I think I was understanding that Cam K can elevate in response to other infections as well. Meaning antibodies to Lyme, myco p, or who knows what else, elevate Cam K. But then I go back to the same old question.....if it's the immune system that is messed up, and thinks the brain is strep, lyme, myco......well, the brain is not going to go away, so won't that signaling continue. Those rogue antibodies (self-antibodies) are not targeting the brain instead of the strep (or other) antigen. How will they ever stop going strong, other than a lobotomy?

 

Alex, LLM, Buster...or anyone with a scientific mind....can you please go into how the anti-neuronals are involved in this picture? As I understand (from a neurologist we saw for a second opinion), your average Joe walking down the street may have some antineuronal antibodies in his blood at any given time. Even Cunningham's work shows on the graph "normal" people with some antineuronals (or maybe I'm just thinking of her "normal mean" not just being "zero.")

 

Thanks!

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I will totally screw this up, but in very basic terms, my understanding is that regardless of what causes autoimmunity - in lupus, Pandas, RA - that once you have a tendency for an autoimmune reaction, what triggers a flair or episode is inflammation.

 

CamK is a protein that is like the flashing blue light in K-Mart (I am seriously dating myself here). The flashing blue light goes off and shoppers flock to the display to see what the blue light special is. Similarly, CamK II signals/reinforces inflammation and calls antibodies (and/or autoantibodies) to the scene.

 

If you treat the infection, there are regulatory T Cells (the store manager)that eventually call the dogs off and in the process, suppress CamK (dim and then unplug the blue light and the crowd disperses). So that's why you need to treat the infection. I think I'm on solid ground so far.

 

In diseases like lupus or RA, where the root cause of a flair is unknown, all you can do is treat the symptoms. You take prednisone, which turns off the blue light (inflammation proteins). This allows the auto-antibody crowd to disperse and the flair downgrades and subsides - until the next trigger, whatever that may be.

 

In Pandas, we think we know what the root cause/trigger is - strep. If you eradicate the strep infection, eventually CamK II production slows down and the body stops creating more and more auto-antibodies. Things eventually regulate again (anecdotally from research papers - 6-8 weeks post-infection eradication). Yes, the basal ganglia is still there as a potential "antigen" but my understanding is that if there's no other antigen in the body that's causing CamK to be super-produced, things calm down. (The BBB also plays a role, but I don't understand it or anti-neuronals well enough to attempt to discuss).

 

So for those whose kids never return to baseline, assuming auto-immunity and/or inflammation is at play, you have to ask why things aren't calming down. The Pandas auto-immunity reaction as I understand it isn't like a nuclear reaction that will go on perpetually without an on-going catalyst (may be different for other autoimmune diseases - I'm not well read on this). As I understand Pandas/CamK, something is still keeping inflammation markers elevated and you need to keep searching for the antigen. Lyme, myco, parasites, yeast, mono, viruses - could all be potential culprits. The lion will roar until you remove the thorn from his paw. Our LLMD believes that if you remove the thorn (and resulting inflammation), my son's auto-immune issues will resolve. That he may not have true auto-immunity. Rather, we're seeing a perpetual response to neuro-inflammation and if we eradicate the lyme and support the body, everything may resolve. I don't think anything is well known at this point.

 

There are several inflammation markers we've tested for my kids - C3a, C4a and C3d immune complexes, MSH (melanocyte stimulating hormone), CamKII - and when all continued to be elevated, we knew that an infection was still at play, beyond strep. For my Pandas son (CamK 183), this led to lyme and pyroleuria. For my daughter (CamK 178 - no strep), we are still trying to find that needle in a haystack root cause while we manage her symptoms.

 

I know others have a much better grasp and maybe they'll add to or correct my analogies.

Edited by LLM
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Alex---wow! That is exactly what I was thinking about this morning....the usual. Wake up. Sigh. STart thinking about pandas. Make breakfast. Think about pandas. Or pitand. or pans. or whatever the @#$& it is anymore. But what I was thinking is that I am a scientific person. I need the science behind it. So thank you for putting it in the beautiful nutshell.

 

LLM---I agree...I think I was understanding that Cam K can elevate in response to other infections as well. Meaning antibodies to Lyme, myco p, or who knows what else, elevate Cam K. But then I go back to the same old question.....if it's the immune system that is messed up, and thinks the brain is strep, lyme, myco......well, the brain is not going to go away, so won't that signaling continue. Those rogue antibodies (self-antibodies) are not targeting the brain instead of the strep (or other) antigen. How will they ever stop going strong, other than a lobotomy?

 

Alex, LLM, Buster...or anyone with a scientific mind....can you please go into how the anti-neuronals are involved in this picture? As I understand (from a neurologist we saw for a second opinion), your average Joe walking down the street may have some antineuronal antibodies in his blood at any given time. Even Cunningham's work shows on the graph "normal" people with some antineuronals (or maybe I'm just thinking of her "normal mean" not just being "zero.")

 

Thanks!

 

Hi eljomom,

 

Great questions. I don't know. I see what you are saying. If the immune system thinks it is finding step when it is really finding brain tissue that it thinks is strep, how do you break the cycle. One thing I think makes sense though, if you actually have an active infection of strep or lyme or whatever, or you are constantly getting reinfected, there is no way you are going to get rid of PANDAS. In my son's case, he had a really bad strep infection to kick off PANDAS, and it wasn't treated at all until 6 weeks after the active infection wound down and he had full blown PANDAS. Since then he has been on continuous antibiotics and still we can't get his ASO titer to come down to the normal range. Is it because the strep is in his tonsils or somewhere that the antibiotics can't get it, or is it just the autoimmune cycle that we haven't been able to halt? At this point for us, I think we can't rule out the tonsils, especially since for some of these kids, removing them works. I think the Psychiatrist who wrote the articles is too confident in his belief that there is an easy answer to PANDAS, but on the other hand, it sounds like he has had some successes, even with adults. For us it is just a matter of leaving no stone unturned.

 

Hi old PANDAS friends! Wish I was on here under better circumstances.

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I will totally screw this up, but in very basic terms, my understanding is that regardless of what causes autoimmunity - in lupus, Pandas, RA - that once you have a tendency for an autoimmune reaction, what triggers a flair or episode is inflammation.

 

CamK is a protein that is like the flashing blue light in K-Mart (I am seriously dating myself here). The flashing blue light goes off and shoppers flock to the display to see what the blue light special is. Similarly, CamK II signals/reinforces inflammation and calls antibodies (and/or autoantibodies) to the scene.

 

If you treat the infection, there are regulatory T Cells (the store manager)that eventually call the dogs off and in the process, suppress CamK (dim and then unplug the blue light and the crowd disperses). So that's why you need to treat the infection. I think I'm on solid ground so far.

 

In diseases like lupus or RA, where the root cause of a flair is unknown, all you can do is treat the symptoms. You take prednisone, which turns off the blue light (inflammation proteins). This allows the auto-antibody crowd to disperse and the flair downgrades and subsides - until the next trigger, whatever that may be.

 

In Pandas, we think we know what the root cause/trigger is - strep. If you eradicate the strep infection, eventually CamK II production slows down and the body stops creating more and more auto-antibodies. Things eventually regulate again (anecdotally from research papers - 6-8 weeks post-infection eradication). Yes, the basal ganglia is still there as a potential "antigen" but my understanding is that if there's no other antigen in the body that's causing CamK to be super-produced, things calm down. (The BBB also plays a role, but I don't understand it or anti-neuronals well enough to attempt to discuss).

 

So for those whose kids never return to baseline, assuming auto-immunity and/or inflammation is at play, you have to ask why things aren't calming down. The auto-immunity reaction as I understand it isn't like a nuclear reaction that will go on perpetually without an on-going catalyst. Something is still keeping inflammation markers elevated and you need to keep searching for the antigen. Lyme, myco, parasites, yeast, mono, viruses - could all be potential culprits. The lion will roar until you remove the thorn from his paw. Our LLMD believes that if you remove the thorn (and resulting inflammation), my son's auto-immune issues will resolve. That he may not have true auto-immunity. Rather, we're seeing a perpetual response to neuro-inflammation and if we eradicate the lyme and support the body, everything may resolve.

 

There are several inflammation markers we've tested for my kids - C3a, C4a and C3d immune complexes, MSH (melanocyte stimulating hormone), CamKII - and when all continued to be elevated, we knew that an infection was still at play, beyond strep. For my Pandas son (CamK 183), this led to lyme and pyroleuria. For my daughter (CamK 178 - no strep), we are still trying to find that needle in a haystack root cause while we manage her symptoms.

 

I know others have a much better grasp and maybe they'll add to or correct my analogies.

 

Hi Laura,

 

Great explanation! Thanks so much. We also are still looking for that damned needle in the haystack. How is your son doing?

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