hot off the press

[eljomom]

I am trying to wrap my head around the 4 anti-neuronals too. I understand cam K can be elevated by other things, but the antibodies are different??? When dr. latimer saw my daughter's, she knew right away that tics were her main issue based on the high anti-D1 antibodies. Anti-D2 was normal. Still wondering how this differentiates TS from pandas. Also, I doubt the auto-antibodies are directly strep related, because my daughter was having major tics (still is) and there was no strep recently leading up to it---just a high fever for one day (NOT STREP) and some STAPH impetigo was running around the house too.

[PacificMama]

Hi Momcap,

I was not necessarily referring to this study re the rise and fall of camk, but more her current work. Likely the findings will be replicated. I was somewhat referring informally to the findings of people here, and wondering if there was some sort of tracking. I do not know the specifics of tracking Dr. C is doing currently. (but as an aside, my daughter was nearly symptom free at the time of her draw, and still she had the high numbers).

 

Regarding those studies you cited and lyme, here is a snippet of what Dr. C passed along to me at some point:

You might assume that in the Lyme sequelae you may expect similar to the cases in these two papers.

Of course, her research now includes testing lyme patients to verify the replication.

 

And as to the antineuronals, I hope others will verify that these are not specific to strep (although those earlier studies did indeed study strep subjects).

 

Someone else would have to verify, but I'm not sure that there are any publishings re the Cunningham study on the tracking of this sort of data (the rise and fall of camK/ antineuronals as it relates to symptom resolution or exacerbation?).

 

Page 6, 2nd paragraph, 2nd sentence: "...antibodies from acute PANDAS sera taken in the symptomatic phase of disease activated CaM kinase II in human neuroblastoma cells. Matched convalescent sera, obtained in the absense of symptoms, did not activate CaM kinase II in comparison to acute sera."

 

I have been reading this study over and over and over again. DS7 has confirmed strep issues (high ASOs), but I also suspect lyme. I'm trying to get my head around what all of this means. I know that other things can cause high CaM K, but I thought the 4 specific anti-neuronal antibodies being studied here are specific to strep. Can someone correct me if I'm wrong? In the study they are referred to as "antibodies directed against an epitope of the group A carbohydrate of Streptococcus pyogenes", and later "antibodies against the streptococcal associated epitope G1cNAc". Does anyone have a study or quote confirming that other infections can lead to production of these particular antibodies?

[momcap]

When dr. latimer saw my daughter's, she knew right away that tics were her main issue based on the high anti-D1 antibodies. Anti-D2 was normal.

 

Well I'm more confused than ever. My DS has elevated anti-D1 (4000) and no motor tics. He's never had motor tics, just lots of mood lability, OCD, and anxiety. I can't wait until she publishes the current data!!!

[philamom]

My dd(9) Anti-neuronal Antibody Titers were all elevated when we had the test done in June 09. A year later we found out she had Lyme.

 

Anti-Lyso 320

Anti-D1 4000

Anti D2 16000

Anti-tubulin 2000

[norcalmom]

My understanding is that these antibodies do no attack strep...they attack neurons - your own body. The strep looks very much like certain neuornal structures we have. That is what "molecular mimicry" refers to.

 

I think Cunninghams is trying to find out if symptoms correlate to specific anti-neuronal antibodies...or if specific types of infection correlate to specific anti-neuronals.

 

I did get an email back about the Cam K and they said they don't know how long it takes to fall in "normal" sera after strep is treated. IT would have been nice and uncomplicated if normal kids with strep didn't produce Cam K. but it is what it is.

 

They did not tell me if strep also raises anti-neuornals (Cam K is not an anti-neuoronal) . I'm sure they have started testing for them in "normal" kids with strep, but I think testing kids that have strep and no neuro psych symptoms is new, so they are still collecting data.

It seems that this new information could mean a few different things.

 

 

"to determine if pandas serum IgG reacted with Lysoganglioside Gm1 and GlcNAc, a competitive inhibition ELISA was utilized. 73% (11/15) of pandas sera binding to GlcNAc-BSA was inhibited by soluble lysoganglioside. In contrast only 23% (6/26) of non-pnadas sera were similarly inhibited. Lysogangliosides concentrations required to inhibit binding of pandas sera were significantly lower than non-pandas sera"

 

To me that means that they put pandas IgG in with Strep (GlcNAc) and Lystoganglioside. ..and the pandas IgG attached to the lysoganglioside instead of the strep(the GlcNAc). (or at least is was not binding to the GlcNAc -i.e. it was "inhibited" by lysoganglioside.)..so I think that shows that pandas sera contains an antibody that likes attaching to Lysoganglioside. Competitive-inhihibition is like a contest to see who the anibodies will pick... will it pick the strep antigen (GlcNAc) or will it pick the Lysoganglioside?

 

AND (again my understanding..which could be very wrong!)(this is not fromt he study, but form reading the forum and other stuff) the way the immune system works is it will get positive feedback for making this error- and keep producing this "rogue" anti-body (anti-neuronal antibody) because it thinks it is doing a good job. It found somehthing to attack (bind to), so, keep sending out more of that type of antibody.

 

FOR those interested in Lyme - Here is something I just came across trying to find more on lysoganglioside normal functions...didn't find that answer, but did find abstract about post lyme syndrome (or chironic lyme syndrom) interesting...and anti-nueronals. (Lysogangliosdie and others)

 

http://www.ncbi.nlm.nih.gov/pubmed/20227484