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help w/ Cunningham Panel and infectious test results & interpretation?

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We finally have DS16's Cunningham Panel, IgeneX, and other lab results. Given the elevated CaMKII, there is definitely an autoimmune reaction, but it's not clear to me

  • how intense, and
  • whether any of the pathogens he tests positive to are likely to be the culprits, or if we need to look further.

Cunningham panel: test = value (normal range; mean)

  • DRD1 IgG = 500 (500-2,000; 1,056)
  • DRD2L IgG = 4,000 (2,000-8,000; 6,000)
  • LYSO-GM1 = 80 ( 80-320; 147)
  • anti-Tubulin = 1,000 ( 250-1,000; 609)
  • CaMKII = 184 ( 53-130; 95)

The Ca++/Calmoudin-dependent protein kinase (CAM KII) activation seems high. But how high is it? Moleculera Lab writes that they now have a database of over 1000 patients, but their attached 2006 paper by Kirvan, Swedo, Snider, Cunningham only shows data on their first 16 PANDAS patients. DS's levels are higher than all but two of those reference kids with acute PANDAS, and almost as high as that in kids with Sydenham's chorea, but is that high enough to impress someone like Swedo or Dr. K? And more importantly, insurance companies to approve IVIG?


I'm also fuzzy on how CAMKII activation would acount for the extreme anxiety, multisensory integration, choreiform movements, pessimistic thinking and other symptoms.

Causative agents: MDL / IgeneX, stool pathology, etc:


The good news is that there's no sign of Lyme or coinfections by ELISA or Western blot.


He does have elevated antibodies to some pathogens (EBV, HHV-6, west nile virus, Mycoplasma) but PCR is negative. Does that mean those area all past infections, or simply dormant at the moment?


For example, here's Epstein-Barr virus, tested in 11/2011 and 2016 Also tested now through MDL, which give unit-less index values, plus they test for virus fragments by PCR.


MDL index
2011 2016 normal (neg <= 0.89, pos >=1.10)

EBV EA IgM 0.52

EBV EA IgG 39 41 <100 u/mL 0.48

EBV VCA IgM 4 18 <100 0.09

EBV VCA IgG 1030 H 971 H <100 4.88


EBV EBNA IgG 444 H 510 H < 100 1.83

EBV RT PCR negative


OK, how to interpret this? I thought IgM disappears after a few months, not that there are low residual levels. And that IgG ought to drop with increasing years since an infection unless there are reactivations. So:

  • Does a +15% in EBNA and quadrupling in IgM simply show uncertainty in lab results, or that there have been some reactivations since?
  • Since EBV RT PCR is negative, does that mean we need not worry about EBV as a causative agent for his PANS, or simply that there's not been a reactivation the last month?
  • How can there be such a difference between the two labs? I'd assumed the index is simply an absolute value / normal level, which fits the EA IgG, but not the VCA or EBNA values.

Similarly, Mycoplasma pneumoniae:

2016 normal MDL index:

IgM EIA 78 <770 0.38

IgG EIA 1.21 <0.90 1.43

PCR negative


Does this indicate a distant infection? I read that IgM can last up to a few months, so I'm surprised to see any level of IgM. Unless it too can establish a latent intracellular infection, as theorized.


Still, there are no smoking guns here. Ditto for HHV-6, West Nile Virus.

The only other things that fournd were MARCONS in Dec, and 4+Mucoid Escnarchia coli and 3+ Citrobacter freundi complex in stool parastiology.


Where do we go from here?




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My kids' CamK's were 179 and 183 and were considered very high - though I do know a few kids who were near or over 200.


CamKII is a cytokine and activates inflammation. In Pans, it causes a cascade of responses, especially in the basal ganglia and amgydala. The basal ganglia is responsible for emotional regulation, sensory attention and prioritizing input. It's the conductor of the orchestra. When data comes into the brain, the basal ganglia decides if it's important. If it is, it forwards that information on to the area of the brain that processes that information. So decisions - that gets sent to the prefrontal cortex. The hum of the refrigerator - not important. Ignore it. Sensory data that is important? Send it on to the parietal lobe. So when the basal ganglia is inflamed, messages get miscommunicated, fears that would normally be dismissed (did I turn off the oven?) get caught in a loop. Memories that need to be recalled - particularly math facts? It's like someone took the card catalog and emptied it all onto the floor. Cam KII plays a particularly important role in memory.


Reading the Wiki pages on the amgydala and basal ganglia and CamK II helped me understand how chronic inflammation easily causes all the things we see in our kids.


Did you run a western blot thru Igenix?


The thing about IgM and IgG - traditional sources will say that it's black and white. IgM is sign of current, IgG is sign of past infection. But some researchers and clinicians who deal with chronic infections report that IgM will cycle in a chronic infection, going through multiple periods of appearing active and that if other signs point to evidence of infection, IgM and IgG alone can't be used to determine what's "active." I don't have any references for you on this - just what I've picked up over time. So I toss it out as food for thought not as authoritative. I'd say to call the lab as ask your more specific questions. as they often have a doctor available to help and who understands the lab's methods and results.


Your question about mycoplasma becoming latent - you may like Stephen Buhner's book on treating mycoplasma. Regardless of your thoughts on herbal treatments, he has a very, very in-depth discussion on how mycoplasma behaves in the body, how it can invade immune cells and become invisible to the immune system, rendering IgG and IgM measurements meaningless. Its the best, most in-depth explanation I've ever come across. For someone with your knack for research, I highly recommend it. http://www.amazon.com/Healing-Lyme-Disease-Coinfections-Complementary/dp/1620550083/ref=sr_1_2?ie=UTF8&qid=1456434679&sr=8-2&keywords=buhner


Don't underestimate the MARCONs. It's played havoc with my DD for a year now. I'm currently feeling there must be something in addition that we're missing (which brought me to Buhner's book). But it's still one more thing she's fighting. This paper specifically mentions both mycoplasma and staph as Pans triggers http://www.jci.org/articles/view/80792

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