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cunningham keynote at conference this Sat


norcalmom

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Anyone going to the conference this weekend? I know its lyme, but its Cunningham speaking as the keynote. I was really diassapointed with the CD I bought from the OCD conference where she presented, she had no time and flew through all this very complex stuff (an hour's presentation done in 10 minutes). Presentations ran over, and she had to leave to catch a plane.

 

Yes it's a Lyme conference. I don't care. She is talking about autoimmune response to infection and antineuoronal antibodies, molecular mimicry...the same tests and studies that she is doing with strep...you say poe-panda and I say poe-lymes disease...(sorry, too much coffee today).

 

I'm not interested in the debate of intial cause, more interested in her tests and studies showing infection and brain interaction..the only test we have to prove its not "all in our heads".

 

Its in Philly at 8:15 (or 8:30) on saturday.

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I will be very interested to hear what's up in Lyme-land since our recent dx. Can't go, though. I sent her and Kathy Alverez an email with an FYI, Evan has lyme, thought you'd like to know since you have tested his blood 2x-184% CaM and anti-lyso elevated. Said I'd be happy to email additional info if it would be helpful. I have always heard back from them the few times I have contacted them. Just thought this is strange--any thoughts why this might be. research reasons? I know there is a real concern of the recent lyme uptick muddying the PANDAS water and possibly derailing research. Just wonder if anyone else has had this same thing happen since being dx'd with lyme after a PANDAS dx. Dr. K did not respond, either. (He has treated Evan).

 

Dawn

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Anyone going to the conference this weekend? I know its lyme, but its Cunningham speaking as the keynote. I was really diassapointed with the CD I bought from the OCD conference where she presented, she had no time and flew through all this very complex stuff (an hour's presentation done in 10 minutes). Presentations ran over, and she had to leave to catch a plane.

 

Yes it's a Lyme conference. I don't care. She is talking about autoimmune response to infection and antineuoronal antibodies, molecular mimicry...the same tests and studies that she is doing with strep...you say poe-panda and I say poe-lymes disease...(sorry, too much coffee today).

 

I'm not interested in the debate of intial cause, more interested in her tests and studies showing infection and brain interaction..the only test we have to prove its not "all in our heads".

 

Its in Philly at 8:15 (or 8:30) on saturday.

I like your attitude. I hope some folks post about this!

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Dawn,

 

I did hear back from Madaleine Cunningham regarding this issue. She did state they were identifying elevated CaM Kinase with individuals diagnosed with Lyme Disease. I understand she is also noting this information on results received by the parents of children recently tested for CaM Kinase.

Edited by SF Mom
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Dawn,

 

I did hear back from Madaleine Cunningham regarding this issue. She did state they were identifying elevated CaM Kinase with individuals diagnosed with Lyme Disease. I understand she is also noting this information on results received by the parents of children recently tested for CaM Kinase.

 

 

SFMom--

Can you elaborate on this -- Do you think she means that the Cam Kinase levels are raised in the case of lyme then? How then does one tell the difference? thanks--

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From what I understand, it is becoming clearer that the CaM elevation is not PANDAS specific. Everyone needs to remember that what she is doing is research--sometimes research can take a turn, or a jog. Maybe these PANDAS/lyme kids hold a unique clue as to what is going on. She is looking into the lyme/CaM connection--my understanding. What will be interesting is the degree of CaM elevation in Lyme vs PANDAS serum. Dawn

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From what I understand, it is becoming clearer that the CaM elevation is not PANDAS specific. Everyone needs to remember that what she is doing is research--sometimes research can take a turn, or a jog. Maybe these PANDAS/lyme kids hold a unique clue as to what is going on. She is looking into the lyme/CaM connection--my understanding. What will be interesting is the degree of CaM elevation in Lyme vs PANDAS serum. Dawn

And she has found 4 antineuronal antibodies that interact w/ basal ganglia- but nobody knows how many more there may be, or what other phenomena may be behind elevated CamKII activity.

Edited by peglem
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What will be interesting...is the whole thing!!

 

I'm dying for her to start publishing some information on what she is finding. She is looking at hundreds of blood samples - from strep related to lyme related...all causeing the same neuro-phychiatric reactions. And, she is getting data on these levels before treatment, and after treatment...after ivig, after antibiotics.

 

IMO once we get rid of the name pandas - we will all be in the same boat. Bacterial infections that trigger neuor-psyciatric symptoms. For some it is lyme, for some it is strep, for some it is mycoplasma. And for some, it can start with one, and then the others do the same. As we know, strep is everywhere.

 

So, if lyme started it...strep can also trigger it in that child. Shouldn't we all be checking for all three know triggers to make sure the underlying infection is gone? I mean...geesh...the amount of tests I've run are astronolical, if I had started with a cunninghams test, and then done titers, lyme and mycoplasma ... that is a drop in the bucket compared to the full allergy, celiacs, funguses, mercury, lead, CBC, immune panels, stool tesing...

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I just asked the same question when I sent in my second kit (for dd10). I said his brother has now dx with Lyme, and I suspect dd has it too, but they both show very clear increase in symptoms when exposed to strep, so my question was simply how does Lyme Disease play in the mix. I'll post when I hear back.

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I have always wondered if they have done enough CamK testing in the general population to establish a real baseline...

Wouldn't they have to test large numbers of the general population what is a truly normal CamK level?

 

I think we tend to understand our kids' CamK numbers of 160, 180, 200 using our understanding of a standard Bell curve, but I am not 100% sure that this applies.

 

Does anyone know if the "average" number truly is 100, and what measures have been taken to get a control group?

 

It's like when I brought up my son's failure of 13/14 pneummocccal titers to someone, I think Dr. L... she said she can't really derive any meaning from them because those titers are not routinely checked in the general population.

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Im looking at the study right now. The non-pandas median was 93. HOWEVER, "normal human sera"(no ocd or tic or adhad)was 108. This is becuase she used a bunch of tics and ocd and adhd sera in the study.

 

When you look at the "normal human sera"(no ocd or tic or adhad) and break out the non-panda ocd, tics and adhd the median goes UP! (you would think it would go down..but probably due to small sample sizes)

 

The range of sera put into the pandas symptom group was 108 to 198. The non-panda range was 50 - 135..that low number (50) was a kid with tics, but not pandas. So, normal and pandas overlap. I'm not sure what she considers to be "pandas range" for the results she is now giving out. I know my son is in it, but he is almost in SC range.

 

The ocd group, seems to be significantly below the normal human sera - at 83. There are six very tightly grouped (75-85) samples in that group.

 

the sample sizes are just too small. For example, the "normal human sera" was only 5 samples.

 

Syndenham chorea was 193- 248...six samples in that group.

 

This study was 2006. I wish she would publish new numbers. She probably has realy good sample sizes now. And now that she knows lyme can trigger it too is probably breaking out lyme, mycoplasma, and strep sera to see if they have different cam K or anti-neuornal numbers.

 

 

She also has "convalescent" numbers in there - but doesn't say how they got to be convalescent. (antibiotics, ivig, pex, time?) or when those samples were taken in raltion to when the acute phases were taken (2 mons post ivig for example?) two of the panda "convalescent" sera are the same as the accute sera...but most go way down. I wonder what accounts for this? perhaps those kids had remission of symptoms on PEX, or anibitotics alone (and just weren't in exacerbation at the time of the draw), where as the others had IVIG? The study doesn't say...that might show that one of the treatments is closing the BBB, but not effecting the sera.

 

there is another interesting statement in the discussion part of the paper...this regarding lysoganglioside (the only anit-neuornal antibody mentioned in the study, although she now is measureing for 3 more) : "All S.C. sera, and 73% of pandas sera possessed GlcNAc-specific IgG that were cross reactive with lysoganglioside. This compared with ony 24% of non-pandas sera. Non-inhibited sera antibodies are presumed to be glNAc-specific antibodies that have no cross reactiviity to lyso.g. We believe that SC and a majority of pandas patiens possess subsets of GlcNaAc specific IgG that cross reacts with lyso.g. that are likely to be involved in the pathogenesis of these disorders which are not thought to be characteristic of other strep infections."

 

this is interesting to me because my ds had only high lyso.g numbers...his other anti-neuroals were in normal range (altho a couple were many times higher than the negative controls). He was not in exacerbation where we took his blood, as a matter of fact his symptoms were almost subclinical at the time. I know she told me that in exacerbation the camKII numbers are higher, but what about the other anti-neuronals?

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