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We use 60mg/day CoQ10, but only because I assume DD11 suffers from the mitochondrial disfunction so common in lyme patients. We noticed no real difference in her behaviour, but we started so many different things at once when she started treatment. My husband takes it daily (he is on statin therapy), and I began using it myself a while back. When I first started supplementing with CoQ10 I noticed an improvement in cognition, but I now find that starting or discontinuing it makes no real difference.

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Thank you very much. First, as another post suggested I/Dr. Lewis tested him for Lyme. It was negative. If the lesion is simply scarring (or other and not cancerous) then I guess I have proof that he actually has/had/will have PANDAS/PANS. Sounds odd to say that, but may need to prove my case for future treatment from traditional local doctor when we are unable to travel to Columbus.

 

I have to explain this to him, friends, family, doctors, social workers, future teachers (he is home schooled at the moment), coaches, and most importantly future partner (and their family). I am trying to make sense of it myself.

 

If 50% have this residual lesion at exactly the basal ganglia, then future 'outlook' should be something predictable.

 

If ever mainstream doctors needed MORE than just 'symptoms' this is it.

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When I see the word lesion - I think MS. And I know at every conference MS is talked about, and to me, very similar to pandas because they know there is a breach of the BBB. Its one of the reasons we take D3 - its the one treatment that is pretty overwhelmingly related to MS. to the point were MS is almost non-existent near the equator. Thank you for post - and please keep us updated on your treatments.

 

I'm confused about the paper that was posted. It says:

Twelve of 17 children (aged 0.4–15 years, nine males) with basal ganglia encephalitis had elevated immunoglobulin G to extracellular dopamine-2 receptor, compared with 0/67 controls

he 12 dopamine-2 receptor antibody-positive patients with encephalitis had movement disorders characterized by parkinsonism, dystonia and chorea. lesions localized to the basal ganglia in 50% of THOSE patients.

 

Elevated dopamine-2 receptor immunoglobulin G was also found in 10/30 patients with Sydenham’s chorea,

 

4/44 patients with Tourette’s syndrome. No dopamine-1 receptor immunoglobulin G was detected in any disease

 

0/22 patients with paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection

 

 

I wish I could read the whole paper. Looks like it is saying that if you have a SEVERE pandas case, and take blood test for anti-dopamine 2 antibodies , and they are high - you most probably have encephalitis, (or a small chance of haing Syndenhams chorea or tourettes...) BUT NOT PANDAS - you have "graduated" from pandas to encephalitis - and need to be evaluated for that??

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When I see the word lesion - I think MS. And I know at every conference MS is talked about, and to me, very similar to pandas because they know there is a breach of the BBB. Its one of the reasons we take D3 - its the one treatment that is pretty overwhelmingly related to MS. to the point were MS is almost non-existent near the equator.

Just a note - the correlation between D3 levels and MS prevalence does not prove causation. Low D3 levels are also common in lyme infection, perhaps being used by the body to fight infection. Lyme is a disease mostly found in temperate regions, it causes brain lesions. The bacteria does not tolerate tropical temperatures.
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Found great article with the help of many.

 

Fluorescent immunohistochemistry demonstrated specific binding to large striatal neurons. Antistreptococcal serologies (both ASO and ant- DNAse B) also were significantly elevated in the subjects. MRI showed hyperintense lesions on unenhanced T2 scans. (T1 sequences were normal.)Eight of 10 children had lesions of basal ganglia,including caudate, putamen, and globus pallidus. Other deep gray structures, as well as supratentorial white matter, brainstem, cerebellum, and cord were involved in some cases (Dale et al., 2001). Although they were quite ill, 8 of the 10 children recovered completely – some after relapses – though one was left with chronic obsessive-compulsive symptoms. Infantile bilateral striatal necrosis, a disorder characterized by abnormal movements and basal ganglia

abnormalities, has also been reported to occur subsequent to GAS infection (Dale et al., 2002).

 

 

A positive outlook until we get more information confirmed.

 

Source: intramural.nimh.nih.gov/pdn/pubs/pub-13.pdf

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MRI showed 3 small lesions on my son's brain. Was done several years ago - I do not remember where the lesions were. He has since been diagnosed with Lyme in addition to PANDAS.

 

Primary symptoms were dilated pupils, dystonia, raging, OCD, loss of math skills, tics, others...

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When I see the word lesion - I think MS. And I know at every conference MS is talked about, and to me, very similar to pandas because they know there is a breach of the BBB. Its one of the reasons we take D3 - its the one treatment that is pretty overwhelmingly related to MS. to the point were MS is almost non-existent near the equator. Thank you for post - and please keep us updated on your treatments.

 

I'm confused about the paper that was posted. It says:

Twelve of 17 children (aged 0.4–15 years, nine males) with basal ganglia encephalitis had elevated immunoglobulin G to extracellular dopamine-2 receptor, compared with 0/67 controls

he 12 dopamine-2 receptor antibody-positive patients with encephalitis had movement disorders characterized by parkinsonism, dystonia and chorea. lesions localized to the basal ganglia in 50% of THOSE patients.

 

Elevated dopamine-2 receptor immunoglobulin G was also found in 10/30 patients with Sydenham’s chorea,

 

4/44 patients with Tourette’s syndrome. No dopamine-1 receptor immunoglobulin G was detected in any disease

 

0/22 patients with paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection

 

 

I wish I could read the whole paper. Looks like it is saying that if you have a SEVERE pandas case, and take blood test for anti-dopamine 2 antibodies , and they are high - you most probably have encephalitis, (or a small chance of haing Syndenhams chorea or tourettes...) BUT NOT PANDAS - you have "graduated" from pandas to encephalitis - and need to be evaluated for that??

 

I think Dale and co. have wonky petri dishes...

according to the Cunningham Testing, my PANDAS dd had very elevated (16,000 H, controls 500-2000) anti-D1 antibodies (associated with OCD?). Her anti-D2 was at the high end of normal 16.000 (normal is 2000-16,0000).

 

"Elevated dopamine-2 receptor immunoglobulin G was also found in 10/30 patients with Sydenham’s chorea, 0/22 patients with paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection and 4/44 patients with Tourette’s syndrome. No dopamine-1 receptor immunoglobulin G was detected in any disease or control groups. We conclude that assessment of dopamine-2 receptor antibodies can help define autoimmune movement and psychiatric disorders. "

Edited by EAMom
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EAMOM -Exactly! - and Tanya Murphy is on the paper, - I know she knows all the cunningham data. Makes me wonder if they are redefining a group of pandas kids as "basal ganglia encephalitis" - exactly how are you suppossed to see basal ganglia encephalitis ?

 

My son also had high D2 - so according to these docs more likely to have BGE (Hey, I like the acronyn - much better than PANDAS!)

 

but I'm thinking its all a matter of semantics. Can't tell without reading the whole paper.

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I'm confused by this, too. My dd also had very, very high anti-D1. Her anti-D2 was within range. Her camK was 187. She had severe OCD AND significant tics/choreiform-movement issues. She was textbook PANDAS presentation, and standard treatments--IVIG, abx, steroids while symptomatic, have brought her back.

 

Wondering, and EAMom hoping maybe you know, if immune deficiencies/low overall immunoglobulins would affect results? Would the levels for someone whose body doesn't produce enough IgG in general be a reliable indicator of elevated or normal levels on a test like this? I don't know enough of the science behind this test to know if that would make a difference. But if it does, I wonder if there've been any studies to determine if SC patients show a similar trend toward low normal to low immunoglobulins as it seems to be fairly common with PANDAS. Also, I wonder if they measured subjects quantitative immunoglobulins, b/c it seems important if that would affect the results. And if it does, and there is a different pattern of quantitative IgG levels between SC and PANDAS patients, wouldn't that impact the interpretation of results? If that info is unknown, seems like some follow-up would be necessary, and might yield more info or clues about what this all means.

 

Will be interested to see what else comes up about this, especially given my dd's somewhat illogical results.

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EAMOM -Exactly! - and Tanya Murphy is on the paper, - I know she knows all the cunningham data. Makes me wonder if they are redefining a group of pandas kids as "basal ganglia encephalitis" - exactly how are you suppossed to see basal ganglia encephalitis ?

 

My son also had high D2 - so according to these docs more likely to have BGE (Hey, I like the acronyn - much better than PANDAS!)

 

but I'm thinking its all a matter of semantics. Can't tell without reading the whole paper.

 

Yes...I wondered about Dr. Murphy being on the paper too.

 

And you wonder if (like Singer) if they even had "real" PANDAS kids, or pseudo-PANDAS kids (who actually had TS, like the ones Singer used).

 

I suspect however, it is something to do with Dale not knowing how to grow stuff in the petri dishes, or having bad cell lines, or something, that is causing his neg results (anti-D1 esp.)

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I'm confused by this, too. My dd also had very, very high anti-D1. Her anti-D2 was within range. Her camK was 187. She had severe OCD AND significant tics/choreiform-movement issues. She was textbook PANDAS presentation, and standard treatments--IVIG, abx, steroids while symptomatic, have brought her back.

 

Wondering, and EAMom hoping maybe you know, if immune deficiencies/low overall immunoglobulins would affect results? Would the levels for someone whose body doesn't produce enough IgG in general be a reliable indicator of elevated or normal levels on a test like this? I don't know enough of the science behind this test to know if that would make a difference. But if it does, I wonder if there've been any studies to determine if SC patients show a similar trend toward low normal to low immunoglobulins as it seems to be fairly common with PANDAS. Also, I wonder if they measured subjects quantitative immunoglobulins, b/c it seems important if that would affect the results. And if it does, and there is a different pattern of quantitative IgG levels between SC and PANDAS patients, wouldn't that impact the interpretation of results? If that info is unknown, seems like some follow-up would be necessary, and might yield more info or clues about what this all means.

 

Will be interested to see what else comes up about this, especially given my dd's somewhat illogical results.

 

I suspect that your dd's results are right. My understanding is that high D1 was seen on PANDAS kids (Cunnigham) and was associated with OCD. High anti-lysogangliosides were associated with pandas tics (don't quote me though).

 

Don't know how immune def would affect results--way over my head, but good question!

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Well, my thoughts are with you during this scary time, and with everyone on this board who has to deal with so much uncertainty. I think it's great that your doctor ordered an MRI. I wish more did because if nothing else it would gather data. We have worked with four of the recommended PANDAS/PANS docs so far and not one has suggested doing any kind of brain scan. I wonder why this is? Regardless, I know it isn't top of your mind but please do keep us posted. All the best!

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MRI showed 3 small lesions on my son's brain. Was done several years ago - I do not remember where the lesions were. He has since been diagnosed with Lyme in addition to PANDAS.

 

Primary symptoms were dilated pupils, dystonia, raging, OCD, loss of math skills, tics, others...

 

Hmmm...so maybe these kids in Dale's paper that have "basal ganglia encephalitis" actually have PANDAS with Lyme?

 

My dd had a MRI a few years back. No lesions were mentioned. It was normal.

Edited by EAMom
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Thank you very much. First, as another post suggested I/Dr. Lewis tested him for Lyme. It was negative. If the lesion is simply scarring (or other and not cancerous) then I guess I have proof that he actually has/had/will have PANDAS/PANS. Sounds odd to say that, but may need to prove my case for future treatment from traditional local doctor when we are unable to travel to Columbus.

 

I have to explain this to him, friends, family, doctors, social workers, future teachers (he is home schooled at the moment), coaches, and most importantly future partner (and their family). I am trying to make sense of it myself.

 

If 50% have this residual lesion at exactly the basal ganglia, then future 'outlook' should be something predictable.

 

If ever mainstream doctors needed MORE than just 'symptoms' this is it.

 

 

Lyme testing tends to be very inaccurate. That's why it's considered a clinical dx, and why an LLMD is needed to really help determine if lyme and co-infections are present.

 

Also, Norcalmom, you mentioned your thoughts about MS. If that's the case, I would not only be looking at the possiblity of lyme et al, but also looking at viruses, particularly HHV-6. There is some possible correlation with Human Herpes Virus-6 and MS and CFS. Both of my children and I have had very high viral loads. After extensive treatment of lyme/co-infections and the immune system as a whole, many of those viruses that were extremely high (IgG in all cases) have come down to normal levels, although we are still fighting some of them. DS-20 has very high HHV-6 IgG for the past year, and we are now doing a viral protocol.

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I'm confused by this, too. My dd also had very, very high anti-D1. Her anti-D2 was within range. Her camK was 187. She had severe OCD AND significant tics/choreiform-movement issues. She was textbook PANDAS presentation, and standard treatments--IVIG, abx, steroids while symptomatic, have brought her back.

 

Wondering, and EAMom hoping maybe you know, if immune deficiencies/low overall immunoglobulins would affect results? Would the levels for someone whose body doesn't produce enough IgG in general be a reliable indicator of elevated or normal levels on a test like this? I don't know enough of the science behind this test to know if that would make a difference. But if it does, I wonder if there've been any studies to determine if SC patients show a similar trend toward low normal to low immunoglobulins as it seems to be fairly common with PANDAS. Also, I wonder if they measured subjects quantitative immunoglobulins, b/c it seems important if that would affect the results. And if it does, and there is a different pattern of quantitative IgG levels between SC and PANDAS patients, wouldn't that impact the interpretation of results? If that info is unknown, seems like some follow-up would be necessary, and might yield more info or clues about what this all means.

 

Will be interested to see what else comes up about this, especially given my dd's somewhat illogical results.

 

I suspect that your dd's results are right. My understanding is that high D1 was seen on PANDAS kids (Cunnigham) and was associated with OCD. High anti-lysogangliosides were associated with pandas tics (don't quote me though).

 

Don't know how immune def would affect results--way over my head, but good question!

 

Just to keep everyone on their toes DS;

cam 160

only D1 elvated 4000..range 500-2000

TICCER...all day all night...i guess some of the tics could be compulsios..but idk..

only ocd that i have finally put a finger on is Triatellanmia..at the start of each allergy season, Starting in february for about a month and then again about august..

Love to hear thoughts on this

Edited by Fixit
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