Psychiatrist on 'Psychlogy Today' website advocates Tonsillect

[eljomom]

So Alex---are you treating just due to ASO? or are symptoms chronic as well? As i understand, some school-age kids run around with elevated titers all the time...maybe just from sheer exposure, whilst not actually contracting strep.

 

LLM--thanks again for taking the time to explain. So truly YEAST can cause inflammation??? The kind of inflammation that reaches the brain?

Also, just trying to connect the dots....the CamK is what causes the formation of auto-antibodies (antineuronals?)

 

Pyroluria? I was tested for that a few years ago...and was high. Tested 2 of my other kids (they both have mild touching oc-tendencies) and one of them now is ticcing. THey were high. Never tested my pandas/pitand kid. Does pyroluria cause inflammation?

[peglem]

Also, just trying to connect the dots....the CamK is what causes the formation of auto-antibodies (antineuronals?)

No- its the antineuronals attaching to receptors on the neurons that raises the CamKII activity. Remember, there is not MORE CamKII in the neurons w/ PANDAS, its just more active because of false signalling(from the antineuronals).

[LNN]

LLM--thanks again for taking the time to explain. So truly YEAST can cause inflammation??? The kind of inflammation that reaches the brain?

Also, just trying to connect the dots....the CamK is what causes the formation of auto-antibodies (antineuronals?)

 

Pyroluria? I was tested for that a few years ago...and was high. Tested 2 of my other kids (they both have mild touching oc-tendencies) and one of them now is ticcing. THey were high. Never tested my pandas/pitand kid. Does pyroluria cause inflammation?

I think yeast can trigger elevated CamK. I know CamK can come from some kinds of gut inflammation. I'm just not certain about yeast can cause the kind of inflammation that results in CamK. I was only trying to list other infections that can cause inflammatory responses. Not suggesting all these things are Pandas triggers. I get myself tied in knots quickly when I got into this sort of discussion. A little knowledge is a dangerous thing.

 

My son was recently tested for kyrptopyroleuria (KPU), which is not a lack of zinc/B6 but rather a defect in the way the blood is synthesized to utilize zinc/B6. As I understand it, you can test blood zinc levels and not see a deficiency, but the body is using the available zinc inefficiently. So you need to mega-supplement. (Think of a guy in one of those cylinders where a cyclone of wind is swirling money around and the guy gets to keep all the money he can grab. There could be millions of dollars in the cylinder but the guy only walks away with a few hundred dollars because he can't grab enough of the stuff he's surrounded by. Measure the cylinder and the answer is there's plenty of money. Measure the amount utilized and you get a different picture). KPU is a urine test. You can read more on the lyme forum or in this paper http://betterhealthguy.com/joomla/images/stories/PDF/kpu_klinghardt_explore_18-6.pdf

 

There are two possible things that could happen as we start KPU treatment today (aside from nothing happening at all). DS could just be zinc/B6 deficient and by giving him supplements, his body and immune system could be energized like taking a drink on a really hot day. Then his now fueled immune system could start fighting lyme more efficiently. Or..his body may have been trying to utilize heavy metals as a poor substitute for zinc, in which case the addition of zinc/B6 could cause his body to drop/chelate the heavy metals as it starts to grab onto the good stuff, in which case it could be a rough spell. The goal in the end would be to have a better functioning immune system to go after the antigen.

 

It is not my understanding that KPU or pyrroleuria cause inflammation in and of itself, but rather that it hinders the immune system, which, in the presence of an infection, would presumably cause increased inflammation. But I'm an art major, not a science geek and I only learn enough to make things make sense in my head. It's very possible that when I connect dots, I miss a few or get a less than complete picture. Always take what I post with a grain of salt. Likewise, KPU and pyrroleuria and the above implications are not embraced by the general medical community. You can google "mauve factor" and find some research but most of it's linked to schizophrenia and is about 30 yrs old. This is one of those gray zones where you take a leap of faith and look for proof in the pudding. We'll do supplements for a few months and see what happens. It makes sense to me, but I can't show you a lot of research to back it up. if anyone has any, I'd love some links!

[eljomom]

peglem....okay, thanks. So then...we need to get rid of antineuronals. Which are circulating because the immune system thinks the brain is the infection....wouldn't this happen even after the infection is gone?

[peglem]

peglem....okay, thanks. So then...we need to get rid of antineuronals. Which are circulating because the immune system thinks the brain is the infection....wouldn't this happen even after the infection is gone?

Okay, this is just pure speculation on my part...I'm thinking of rheumatic heart disease, where the autoantibodies attack heart tissue. In that case, the autoantibodies (made to attach to strep antigens)attach to cells in heart valve tissue and mark them for destruction, just like they mark the strep for destruction. But, once the infection is cleared and the antibodies are cleared, the body does not "see" that heart valve tissue as foreign and continue making antibodies to that tissue. What I think is that the antigens on the bacteria are not exactly the same as the heart valve antigens, but similar enough that the antibodies can attach.

I think the PANDAS thing is similar-except, in this case the autoantibodies are not complexing with basal ganglia cells and marking them for destruction, but are triggering neuronal cell activity, generating false signalling. I don't think the immune system sees receptors on the basal ganglia as foreign. I think its a case of the antibodies to pathogens being similar enough to the substance that is supposed to trigger the cell. So, if the pathogen is gone and the antibodies to it have gone, autoimmunity stops. The body keeps copies of the antibodies, but they don't circulate until the immune system senses a threat (can be just exposure w/o actual infection)and starts producing the specific antibody in large quantities-to keep you from getting infected.

[911RN]

(The BBB also plays a role, but I don't understand it or anti-neuronals well enough to attempt to discuss).

 

 

 

 

OK...I'll take a stab at this one:) The BBB was loong thought by medical establishment to be the sacred cow. Was thought that the brain "protected" itself by the BBB.It was not penetrated by proteins/amino acids (antibodies) like other parts of the body- heart, kidneys etc. It was thought that the BBB was an impenetrable wall. NOT SO. This has been disproven. However, scientists are constantly fighting the BBB believers (of days gone by) to state that if a brain antigen, induced after an infectious trigger, is recognized then immune activation can occur.

 

Alex, love your Kmart blue light shopper analogy. LLM-You are on the right track, too- have a good understanding of the process by my way of thinking:)

 

My take on the whole process and how my brain made sense of it is this: One is exposed to infectious trigger (strep, whatever)- body forms antibodies (which are essentially amino acid proteins)- these cross the BBB- become antinueronal antibodies- reside and attach themselves to brain tissue- live in the basal ganglia in a somewhat dormant state. Just hanging out- (sitting around brain dead, bored, playing Xbox:). Have another infectious trigger (somebody brings the beer)- the residents (Antineuronal antibodies) come "alive" and begin to party and bounce all around the joint- inviting their friends (CamKinase II). The place become overflowed- inflammation causing swelling in the basal ganglia. The place is getting trashed- symptoms of tics, OCD, decline in writing, math skills etc. until the parents or cops show up- antibiotics, IVIG, PEX, removal of the infectious trigger, time, T&A, glutamte blockers, SSRI's etc.

 

That's my simplistic analogy. I think it is also possible for ANA's to live dormant in other parts of the brain- not just basal ganglia. That's why our kids have such differing symptoms. Once they are able to cross the BBB- all bets are off- in my view.

 

In my son's case- speech decline was first symptom. I believe he has/had a party going on in his temporal lobes, as well as, basal ganglia. To the point of abnormal, nocturnal EEG activity in that lobe- although, he has never had a seizure. We calmed down the temporal lobe with Lamcital. Now, attempting to calm down basal ganglia with SSRI? We did 90 days of high dose Azithro in Spring which arrested the motor tics. Which,is primarilly what the high Cam Kinase II causes following Strep. If one follows the path of SC as the role model.However, the quirky, nondebilitating OCD is our final target. Short of PEX, IVIG- I'm not sure one can ever get rid of the antineuronal antibodies?? They are just "there" as a potential source to start the whole neuro-inflammatory process, auto immunity process in the presence of an offending trigger.

 

Maturity and a "grown up" immune system is one theory- reason many of these kids improve with puberty. Reason prophylactic antibiotics are being recommended until age 25 or so. To allow the immune system time to grow up. Using RF as role model.I'm so hoping that is case for us!

 

Alex, my suspected PANDAS DS11 had T&A at age 5.5 for obstructive sleep apnea- PANDAS not even known at that time. Suspect, now, he had PANDAS before and flare following removal. But, I don't regret their removal. Had to be done- don't regret it. My older NT son (14) had adenoids removed at age 12- they were growing into his nasal passages and sinus cavities! Causing severe mouth breathing at night to point it was shortening space between nose and upper lip- which was going to cause dental/cosmetic issues once braces were needed! Showed up on Maxillofacial CT as a "mass". ENT came out and said he had removed "pile"- had two hands opened up of adenoid tissue. This child has likely had one or two PANDAS flares in past that he completely recovered from. He suffered allergies (shots for 5 years), chronic sinus infections etc. I'm sure that adenoid tissue was laden with all manner of bacteria. He has not a had a sinus infection since the adenoid removal! Still has tonsils and still gets strep. Also had Uvelitis twice in the last 2 years (often caused by Homoephalus Infuenza- which is a bacteria, not a virus). I wish they would have taken his tonsils out, too!

 

I'd say if you have two docs telling you to get tonsils out- get them out. They don't recommend it lightly, anymore. Have to see need. Whereas, in the 60's and 70's- everyone seemed to get their tonsils removed? With the "new" finding of PANDAS- not sure that was a bad practice. Only since medicine has insisted on leaving them in has PANDAS been on the forefront.

 

Ask docs to premedicate with ABX if not already on suppression and follow with long course. If infected tissue is what is causing sustained high titer- makes sense to remove the offending organ.

 

Anyway, sorry so long- anyone can feel free to correct my party analogy or incorrect assummptions:0)