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Antibodies to strep throat bacteria linked to obsessive compulsive dis


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Michele, Could he have a lot of residual symptoms from getting sick for so many years? But I think that may only account for the OCD and ODD. I don't know if you can have residual tics. That part wouldn't make sense. That may also explain why the steroid didn't work. Like with Josh. He has PANDAS. He's responded to a steroid burst before so that backs up that he has PANDAS.However, he now has residual OCD. Granted, it's different than Andrew's and it's almost gone, but he also hasn't been sick as long as Andrew. I've now heard from many parents who are in the same situation as me. If Josh did a steroid burst today, would the remaining OCD go away from it? I honestly don't know. I,admit, it would have been fascinating to see if the chemicals in Josh's brain matched those of a person w/ clinical OCD after his PANDAS episode, but prior to today when most the residual OCD is gone.The chemicals in an OCD brain appear different in MRI's. Hmm....what kind of doctor would prescribe an MRI? A neurologist, right? Have you asked Dr Latimer if that would be something to consider?

 

So, anyway, it can also be that Andrew has OCD and TS and PANDAS. The original definition was that PANDAS was a subset of children who already had those disorders. I think at this point, continue to treat the situation as if Andrew does have actual OCD and TS. However, like some one else said look into a different field, like immunology, to tackle the PANDAS problem.

 

Now that you've had the steroid burst, would you consider a consult w/ DR K to get his opinion? I know $ doesn't grow on trees and you just paid a pretty penny for Latimer.

 

Finally, did you ask Dr Latimer whether the meds Andrew were on could cover up any improvement that he might have had from the steroid?

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I do think the TS is a risidual just like the anxiety. I would think the study at NIMH would do the brain study. Latimer said the drugs he was on should be fine with the steroids but she suggested getting him off Abilify because of possible side effects long term. We did consult with Dr. K maybe we could do it in person yet though. We did see two ped immunologists. Both gave the antibiotics. I asked them about IVIG and neither of them had used it for PANDAS. I could seek out a new one. How about those Dr's at Cleveland clinic that list it online with their names and then won't see patients. One immunologist I found in Toledo would do IVIG if a local Dr. whom she knew diagnosed it and prescribed it. When I asked about the name of a neuro Dr. whom she had done it before they said they weren't seeing patients anymore. I bet Dr. K would do it. Maybe Ohio State school of med. OH can't be this behind in med can they?

 

Michele

Michele, Could he have a lot of residual symptoms from getting sick for so many years? But I think that may only account for the OCD and ODD. I don't know if you can have residual tics. That part wouldn't make sense. That may also explain why the steroid didn't work. Like with Josh. He has PANDAS. He's responded to a steroid burst before so that backs up that he has PANDAS.However, he now has residual OCD. Granted, it's different than Andrew's and it's almost gone, but he also hasn't been sick as long as Andrew. I've now heard from many parents who are in the same situation as me. If Josh did a steroid burst today, would the remaining OCD go away from it? I honestly don't know. I,admit, it would have been fascinating to see if the chemicals in Josh's brain matched those of a person w/ clinical OCD after his PANDAS episode, but prior to today when most the residual OCD is gone.The chemicals in an OCD brain appear different in MRI's. Hmm....what kind of doctor would prescribe an MRI? A neurologist, right? Have you asked Dr Latimer if that would be something to consider?

 

So, anyway, it can also be that Andrew has OCD and TS and PANDAS. The original definition was that PANDAS was a subset of children who already had those disorders. I think at this point, continue to treat the situation as if Andrew does have actual OCD and TS. However, like some one else said look into a different field, like immunology, to tackle the PANDAS problem.

 

Now that you've had the steroid burst, would you consider a consult w/ DR K to get his opinion? I know $ doesn't grow on trees and you just paid a pretty penny for Latimer.

 

Finally, did you ask Dr Latimer whether the meds Andrew were on could cover up any improvement that he might have had from the steroid?

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I do think the TS is a risidual just like the anxiety. I would think the study at NIMH would do the brain study. Latimer said the drugs he was on should be fine with the steroids but she suggested getting him off Abilify because of possible side effects long term. We did consult with Dr. K maybe we could do it in person yet though. We did see two ped immunologists. Both gave the antibiotics. I asked them about IVIG and neither of them had used it for PANDAS. I could seek out a new one. How about those Dr's at Cleveland clinic that list it online with their names and then won't see patients. One immunologist I found in Toledo would do IVIG if a local Dr. whom she knew diagnosed it and prescribed it. When I asked about the name of a neuro Dr. whom she had done it before they said they weren't seeing patients anymore. I bet Dr. K would do it. Maybe Ohio State school of med. OH can't be this behind in med can they?

 

Michele

Michele, Could he have a lot of residual symptoms from getting sick for so many years? But I think that may only account for the OCD and ODD. I don't know if you can have residual tics. That part wouldn't make sense. That may also explain why the steroid didn't work. Like with Josh. He has PANDAS. He's responded to a steroid burst before so that backs up that he has PANDAS.However, he now has residual OCD. Granted, it's different than Andrew's and it's almost gone, but he also hasn't been sick as long as Andrew. I've now heard from many parents who are in the same situation as me. If Josh did a steroid burst today, would the remaining OCD go away from it? I honestly don't know. I,admit, it would have been fascinating to see if the chemicals in Josh's brain matched those of a person w/ clinical OCD after his PANDAS episode, but prior to today when most the residual OCD is gone.The chemicals in an OCD brain appear different in MRI's. Hmm....what kind of doctor would prescribe an MRI? A neurologist, right? Have you asked Dr Latimer if that would be something to consider?

 

So, anyway, it can also be that Andrew has OCD and TS and PANDAS. The original definition was that PANDAS was a subset of children who already had those disorders. I think at this point, continue to treat the situation as if Andrew does have actual OCD and TS. However, like some one else said look into a different field, like immunology, to tackle the PANDAS problem.

 

Now that you've had the steroid burst, would you consider a consult w/ DR K to get his opinion? I know $ doesn't grow on trees and you just paid a pretty penny for Latimer.

 

Finally, did you ask Dr Latimer whether the meds Andrew were on could cover up any improvement that he might have had from the steroid?

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I do think the TS is a risidual just like the anxiety. I would think the study at NIMH would do the brain study. Latimer said the drugs he was on should be fine with the steroids but she suggested getting him off Abilify because of possible side effects long term. We did consult with Dr. K maybe we could do it in person yet though. We did see two ped immunologists. Both gave the antibiotics. I asked them about IVIG and neither of them had used it for PANDAS. I could seek out a new one. How about those Dr's at Cleveland clinic that list it online with their names and then won't see patients. One immunologist I found in Toledo would do IVIG if a local Dr. whom she knew diagnosed it and prescribed it. When I asked about the name of a neuro Dr. whom she had done it before they said they weren't seeing patients anymore. I bet Dr. K would do it. Maybe Ohio State school of med. OH can't be this behind in med can they?

 

What I was thinking with immunology or rheumatology was that maybe they could detect some sort of immune disorder or deficiency, not PANDAS, that would justify IVIG. That way, you could still get the treatment, regardless of what they want to call the disorder he is being treated for.

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I do think the TS is a risidual just like the anxiety. I would think the study at NIMH would do the brain study. Latimer said the drugs he was on should be fine with the steroids but she suggested getting him off Abilify because of possible side effects long term. We did consult with Dr. K maybe we could do it in person yet though. We did see two ped immunologists. Both gave the antibiotics. I asked them about IVIG and neither of them had used it for PANDAS. I could seek out a new one. How about those Dr's at Cleveland clinic that list it online with their names and then won't see patients. One immunologist I found in Toledo would do IVIG if a local Dr. whom she knew diagnosed it and prescribed it. When I asked about the name of a neuro Dr. whom she had done it before they said they weren't seeing patients anymore. I bet Dr. K would do it. Maybe Ohio State school of med. OH can't be this behind in med can they?

 

Michele

 

Michele, how about emailing Dr K and writing him everything thats going on? I don't think he charges for responses via email, only for phone consults.

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Michele,

 

Wow, 7 years. We're exhausted at just 1 year. We're post-IVIG by one week and things are actually getting worse, not better. It's very scary. Despite all my reading, I'm not at all feeling qualified to advise you because we are really not through it ourselves.

 

In terms of your questions, yes, prednisone did have an effect. However, in our case, the effect was 10 days after the burst. It was noticable with a complete absence of social anxiety, tics, chorea, measurement rituals or any other symptoms. We were amazed. Then 4 days later, our dd9 was back to her withdrawn self.

 

My gut is that Latimer and others are responding to the long length of illness. We don't know if PANDAS becomes something else long term (such as classic OCD and TS) and in our own child we've seen an increasing baseline when plotted over the past year that isn't corrected with antibiotics. She never seems to fully reset from an exacerbation so the baseline of symptoms between exacerbations just gets higher.

 

I guess the real question for you is whether you see episodes now correlated with strep or whether you are seeing more mild variations. In Kurlan's study of long-term TS/OCD patients -- he saw OCD changes of +/- 1.6 points over 2 years. In Swedo's studes of sudden onset, she saw OCD changes of +/- 20 points (i.e., 10 times larger). I'm not sure whether Kurlan had any PANDAS kids at all, but he'd say they met all the criteria. I'd say they didn't have Swedo's criteria of episodic exacerbations with dramatic onset and fall (i.e., the 20 pts CY-BOC score changes). Perhaps that is what Latimer is responding to if your child is demonstating mostly constant OCD behavior. Of course this could also be the meds doing what they are supposed to. I don't think anyone knows.

 

It seems a really reasonable question to ask your doctors what led them to one diagnosis over another especially since they actually are supporters of treating PANDAS. My gut is that they just haven't seen a kid with 7 years of suffering and are thinking that treating the symptoms will likely require other methods than with onset PANDAS kids. I really wish I knew what to advise you here. Perhaps an email with Dr. K could help as he's probably seen more patients than anyone else and might have a sense for whether the same treatment has been helpful on longer term sufferers.

 

Best regards,

 

Buster

 

 

 

Buster or others who have done research,

My son had strep at 13 months, afterwards a dramatic change and chorea and tics and then later OCD and tics with other exposures. So why would Latimer feel it may be TS or OCD? Doesn't this study prove that predisposition to autoimmune ( I have arthritis) and predisposition to anxiety disorders and mental illness( my husband's side) can be a precurser to PANDAS. He had positive Kinase 11 which were in the low PANDAS range. Why would she be confused to if it was PANDAS? He had a long history waxing and waning with illness for 7 years after illness. Now he isn't responding well to steroids, they seem to aggravate his symptoms, does this prove it is not PANDAS? Did you kids all do well with steroids and how long did it take? We are on day 21. Sometimes he seems easier, othertimes agitated, hyper and raged. The anxiety and tics are increased. The next question, what do we do now? I mean we meet every symptom of PANDAS. The longer it continues it seems to be going into ASD with tics and anxiety. If Latimer is the best to see, she was not convinced so what or who now? She sugested the OCD study at NIMH but it is alot , 11 visits in 6 months, possible placebo, and who knows about the drug side effects anyways? They want you stay on current meds and that is alot of meds for a young boy age 7. Just wondered if you had any opinions?

 

Michele

Just as a reminder, the new paper is a followup to work by the same author in 2004

 

http://www.jneurosci.org/cgi/reprint/24/7/1780

 

that was entitled "A Murine Model for Neuropsychiatric Disorders Associated with Group A -Hemolytic Streptococcal Infection" that heavily cited Kirvan/Cunningham's work on GlcNAc.

 

what was different here was that the authors transferred the created antibodies from immunized mice into non-immunized mice and showed that the transfer of serum caused the movement/behavior issues.

 

The push back on the paper will be similar to the prior paper that "mice aren't people", but wow, it's very good work and very consistent with the findings of Kirvan and Cunningham. It would be fascinating to know whether the innoculated mice have an antibody similar to 24.3.1.

 

Regards,

 

Buster

 

 

http://www.eurekalert.org/pub_releases/200...s-ats081009.php

 

Maybe we are finally, once and for all, going to get this "controversial" disorder recognized!

 

Colleen

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Thanks Buster and all of you for your support.

 

Buster, did you do a 5 day burst? Then 10 days later she improved? Then there is still hope since we are only on day 21. Did you get the IVIG from Dr. K?

 

His daily baseline is definately changed. That is why he now seems more ASD/anxiety daily when he was typical before inbetween. Really our Dr's have called it TS for sometime. Clev Clinic and University Hospital Cleve will not recognize or treat PANDAS. I did have a few Dr's early on at Akron Children's who thought it might be PANDAS and gave him antibiotics. I can not find any local Dr's to treat PANDAS. If I keep searching I am afraid they are about to call me munchausen. The last appointmen was scary. I got the impression the psych thought I was crazy and messing my kid up by putting him through all this. I was actually scared he may call social services. I hope to never see him again.

 

Dr. Murphy in Florida thought it was PANDAS and she was right on in what to expect down the road, but she would not treat him across state lines with meds. The way she suggested meds and not IVIG makes me think they know this is life long. She suggested Tennex, and Clonidine and Ritalin. I wonder if that is what she still uses in these cases of ADHD, anxiety and tics? Has anyone seen her lately, her name seems to have disappeared here?

 

We are on Abilify, Celexa and Clonidine. I wish we could start over on meds but it is tricky to do much like the boy in Against Medical Advice. Somedays I just wish he would wake up and be cleared and we could forever put this battle for searching for answers and Dr's behind us. Then he starts acting out in the first 30 minutes and I know it is not possible. Maybe he will be much better off the steroids. I have really hit a low lately. In the ASD book it says you go through grief after diagnosis and I feel like I am.

 

Thanks again,

 

Michele

Michele,

 

Wow, 7 years. We're exhausted at just 1 year. We're post-IVIG by one week and things are actually getting worse, not better. It's very scary. Despite all my reading, I'm not at all feeling qualified to advise you because we are really not through it ourselves.

 

In terms of your questions, yes, prednisone did have an effect. However, in our case, the effect was 10 days after the burst. It was noticable with a complete absence of social anxiety, tics, chorea, measurement rituals or any other symptoms. We were amazed. Then 4 days later, our dd9 was back to her withdrawn self.

 

My gut is that Latimer and others are responding to the long length of illness. We don't know if PANDAS becomes something else long term (such as classic OCD and TS) and in our own child we've seen an increasing baseline when plotted over the past year that isn't corrected with antibiotics. She never seems to fully reset from an exacerbation so the baseline of symptoms between exacerbations just gets higher.

 

I guess the real question for you is whether you see episodes now correlated with strep or whether you are seeing more mild variations. In Kurlan's study of long-term TS/OCD patients -- he saw OCD changes of +/- 1.6 points over 2 years. In Swedo's studes of sudden onset, she saw OCD changes of +/- 20 points (i.e., 10 times larger). I'm not sure whether Kurlan had any PANDAS kids at all, but he'd say they met all the criteria. I'd say they didn't have Swedo's criteria of episodic exacerbations with dramatic onset and fall (i.e., the 20 pts CY-BOC score changes). Perhaps that is what Latimer is responding to if your child is demonstating mostly constant OCD behavior. Of course this could also be the meds doing what they are supposed to. I don't think anyone knows.

 

It seems a really reasonable question to ask your doctors what led them to one diagnosis over another especially since they actually are supporters of treating PANDAS. My gut is that they just haven't seen a kid with 7 years of suffering and are thinking that treating the symptoms will likely require other methods than with onset PANDAS kids. I really wish I knew what to advise you here. Perhaps an email with Dr. K could help as he's probably seen more patients than anyone else and might have a sense for whether the same treatment has been helpful on longer term sufferers.

 

Best regards,

 

Buster

 

 

 

Buster or others who have done research,

My son had strep at 13 months, afterwards a dramatic change and chorea and tics and then later OCD and tics with other exposures. So why would Latimer feel it may be TS or OCD? Doesn't this study prove that predisposition to autoimmune ( I have arthritis) and predisposition to anxiety disorders and mental illness( my husband's side) can be a precurser to PANDAS. He had positive Kinase 11 which were in the low PANDAS range. Why would she be confused to if it was PANDAS? He had a long history waxing and waning with illness for 7 years after illness. Now he isn't responding well to steroids, they seem to aggravate his symptoms, does this prove it is not PANDAS? Did you kids all do well with steroids and how long did it take? We are on day 21. Sometimes he seems easier, othertimes agitated, hyper and raged. The anxiety and tics are increased. The next question, what do we do now? I mean we meet every symptom of PANDAS. The longer it continues it seems to be going into ASD with tics and anxiety. If Latimer is the best to see, she was not convinced so what or who now? She sugested the OCD study at NIMH but it is alot , 11 visits in 6 months, possible placebo, and who knows about the drug side effects anyways? They want you stay on current meds and that is alot of meds for a young boy age 7. Just wondered if you had any opinions?

 

Michele

Just as a reminder, the new paper is a followup to work by the same author in 2004

 

http://www.jneurosci.org/cgi/reprint/24/7/1780

 

that was entitled "A Murine Model for Neuropsychiatric Disorders Associated with Group A -Hemolytic Streptococcal Infection" that heavily cited Kirvan/Cunningham's work on GlcNAc.

 

what was different here was that the authors transferred the created antibodies from immunized mice into non-immunized mice and showed that the transfer of serum caused the movement/behavior issues.

 

The push back on the paper will be similar to the prior paper that "mice aren't people", but wow, it's very good work and very consistent with the findings of Kirvan and Cunningham. It would be fascinating to know whether the innoculated mice have an antibody similar to 24.3.1.

 

Regards,

 

Buster

 

 

http://www.eurekalert.org/pub_releases/200...s-ats081009.php

 

Maybe we are finally, once and for all, going to get this "controversial" disorder recognized!

 

Colleen

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Buster,

 

I'm wondering now if the carbohydrate composition of the protein was not part of this study? As you pointed out on one of the threads, cost constraints or just not part of what they were interested in proving/confirming?

 

 

Just as a reminder, the new paper is a followup to work by the same author in 2004

 

http://www.jneurosci.org/cgi/reprint/24/7/1780

 

that was entitled "A Murine Model for Neuropsychiatric Disorders Associated with Group A -Hemolytic Streptococcal Infection" that heavily cited Kirvan/Cunningham's work on GlcNAc.

Thinking about that remark, I went back and read the psoriasis study that posted somewhere here already. They know the antibodies recognized two proteins, but further study was needed to determine that the antibodies were directed toward GlcNAC.

 

bolding mine

 

http://pt.wkhealth.com/pt/re/clei/abstract...#33;8091!-1

 

We have previously reported the finding of circulating antibodies recognizing two proteins of 100 and 120 kD (PO100 and PO120) fromPityrosporum ovale in patients with psoriasis.

 

The present study aimed at further characterizing the specificity of these antibodies. Enzyme-labelled lectins were used to determine the carbohydrate composition of PO120 and PO100. BSII, a lectin that recognizes terminal N-acetylglucosamine (GlcNAc), showed the same banding pattern as sera from patients.

Our results are indicative that the antibody response to PO100 and PO120 in patients with psoriasis is directed towards terminal GlcNAc residues.

 

 

What I keep wondering about, is the brief discussion that we had about NAG (the supplement) showing protection againt autoimmune attack. This sentence in the psoriasis /P. ovale study, is something I'm trying to understand.

 

 

Psoriatic sera that were positive in the ELISA against a heat-denatured extract of P. ovale were rendered negative only by pre-incubation with GlcNAc in a concentration-dependent manner.

 

 

Since I don't understand how these tests work, I'm wondering if you have any thoughts on the significance of this?

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Buster,

 

If you read my last post, never mind my question regarding the significance of treatment with GlcNAc.

 

I think what I'm getting out of "binding inhibition Elisa" is that the

proteins on the surface of the microorganism recognize and bind to carbohydrates of host cells. By treating sera of psoriasis patients with N acetylglucosamine, they blocked the adhesion capability because the adhesion site was already occupied, thereby preventing binding with the P. ovale or specifically the GlcNAc residues.

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Buster, did you do a 5 day burst? Then 10 days later she improved? Then there is still hope since we are only on day 21. Did you get the IVIG from Dr. K?

 

We actually did a 6 day burst. And then on day 16 (i.e., 10 days from end of burst) we saw noticable improvements (easy interactions with adults, a carefree cheerfulness we hadn't seen in years, lack of separation anxiety). But it was only temporary (i.e., for 3-4 days). Then back to baseline. In terms of IVIG, our local immunologist ordered it and followed Dr. K's protocol. We do not know what will be covered by insurance (if any).

 

Buster

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Okay that paper is going to take some time to parse. Wow. How'd you find that one :blink:

 

The problem with the Yaddanapudi study is that we're not quite sure if we're reading about symptoms of EAE or about the reaction to the auto-antibodies.

 

It would really help to have an immunology student to bug for a while with questions... I swear if I keep up at this much longer I'm going back and studying immunology ;)

 

Buster

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I went ahead and contacted some groups of immunology graduate students in facebook groups and asked if anyone would be interested, and curious, to visit this forum and help translate some of these studies. Let's see if we get a response.

 

 

 

Okay that paper is going to take some time to parse. Wow. How'd you find that one :blink:

 

The problem with the Yaddanapudi study is that we're not quite sure if we're reading about symptoms of EAE or about the reaction to the auto-antibodies.

 

It would really help to have an immunology student to bug for a while with questions... I swear if I keep up at this much longer I'm going back and studying immunology ;)

 

Buster

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