GMT111

I've been at this for many years, with two kids who are affected - here's my take on it-
 
You contract an infection and your immune system produces antibodies against that infection. So far so good. Then those immune cells migrate into your olfactory bulb (which may happen in all people because the sinuses are a first line of defense for keeping intruders out). But in Pans kids, those immune cells (Th17 antibodies) find a weak spot through the cribiform plate (boney plate that separates your sinus cavity from your brain). Now those antibodies are on the wrong side of your blood-brain barrier, where they don't belong. The brain's immune system (glial cells) react to this invasion and create an abundance of inflammation. It's an attack against self, but an understandable one. Those Th17 cells shouldn't be in the brain. This is what makes Pandas kids different from other kids who get the same infection - that breach of the blood-brain barrier.
 
Once this breach happens, other infections in addition to strep can trigger the same response, and now you have Pans. Research has shown that these Th17 cells can stay active even 2 months after an active infection has been cleared. But in my personal experience, once you clear the infection, the body settles back down and you see symptoms start to resolve.
 
So from a practical standpoint, if the antibiotics have helped your daughter clear her infection, then stopping the antibiotics should be ok. But realize if her body now responds in a Pandas way, she will be vulnerable to additional Pandas flares when she gets future infections. At least until she passes thru puberty - and at that point some kids outgrow it and some don't but seem to get less sensitive, tho still reactive.
 
Some kids who have repeated flares are kept on antibiotics prophylactically. Some are lucky enough to enjoy long periods of being infection-free and can just go on antibiotics quickly at the first signs of behavioral changes and the horse is put back in the barn without long periods of disruption. But the key is to react quickly without relying on strep tests or "proof" on a new infection - because once you have Pandas, it can be many other infections that trigger the same immune response. And even then, one antibiotic doesn't work on every bacteria (e.g. mycoplasma or lyme need different antibiotics than strep) and it doesn't work if the trigger is a viral or fungal infection (yeast, mold, colds, flu). So for kids who have trouble staying healthy, this can be a more chronic situation.
 
It's a delicate balance and you won't know until you stop the antibiotics and see what happens. If you see a return of symptoms right away it may mean that the infection isn't gone. If she seems back to baseline, then you'll need to be vigilant and hopefully have doctors on board who will allow you to put her back on antibiotics at the first sign of Pandas symptoms. But you should probably view this as a long term risk whenever she gets an infection. Pandas isn't a one time event. Once you have the condition, you stay vulnerable any time you have an infection, at least through childhood.
 
But to leave you with a bit of hope...,my son developed Pandas when he was 6. Over 5 years, we had to treat him for strep and Lyme and mold exposure that turned out to be in his elementary school. He spent 5 years on antibiotics. Then 2 additional years going on antibiotics at the first sign of symptoms. He's now 13 and has survived his first winter without any issues, even though he was sick several times. (we've switched to herbal antibiotics that I can have on hand and use quickly without needing to get in to see the doctor and he's old enough that he can recognize early feelings, so our ability to respond is much better now). But he also seems to be outgrowing his vulnerabilities.

PMd you

Also I wonder if you call it its re-branded name: Post infectious autoimmune encephalopathy, will remove the paediatric part (assuming your older) as I think PANS/PANDAS tends to limit the group it affects, my apologies if this is unhelpful, i understand your desperation, I would try the private route.
 
I've attached a paper about auto immune encephalopathy, in it, it describes a number of auto immune anti-bodies as well as the offending infections in this condition, it relates to paeds but equally applicable to adults. If you are able to identify with your GP any of the antibodies for the infections you might just be able to get a decent enough neurologist to acknowledge. My son has current infection for mycoplasma pneumoniae has abx but no doctor to provide ongoing treatment.
 
The research was carried out in England
 
http://jnnp.bmj.com/content/84/7/748.full

We're at our wits' end to find anyone who can treat me - we'd had high hopes of Amy Smith in California but have been unable to get any reply to our calls and e-mails so far.
 
Who do all of you know who will treat PANS in adults? And who's willing to do long-distance consultations? Please name as many of each as you can!!
 
My family doctor is willing to take any blood samples that are needed, write prescriptions on the specialist's instructions (so long as they're not for things that she, at her level of seniority, isn't authorised to prescribe - I don't know how likely that is to be a problem) and be responsible for keeping an eye on my general physical state. I know that that's the eminently sensible-sounding arrangement Amy Smith follows for long-distance patients, but no sooner had we established that than she went incommunicado on us.
 
By the way, if we can find such a person, do you happen to know if there are any particular difficulties to be dealt with in being treated by a doctor in another country? We're in the UK and I know there don't yet seem to be many PANS specialists outside the USA.
 
Thank you all very much in advance,
Wombat140

Any MD can request a MarCONS collection kit and follow the instructions. However you need a doctor who will be careful to keep the swab from contacting the mucus membranes at the front, and pay attention to how deep to go and how much to brush the membrane.
 
We had it done by a Lyme/PANS doctor. I have never had a general ENT or internist suggest these. It's not a term used generally, and no consensus that this is important, so 3-week nasal cultures are not standard. But it's not completely crazy.
 
Here's more information on MarCoNS, the theory, and a few references that gave it (to me) enough plausibility, though they don't at all prove that MarCoNS are the culprits in PANS.
 
MarCoNS is a name used by Dr. Shoemaker to describe slow-growing multi-drug-resistant COag-Negative Staph found deep in the nasal cavity, which he believes cause chronic illness. A prominent member is S. Epidermis, which is found everywhere on our skin, outer part of the nostrils, esp. armpits -- and is considered to be benign except when it colonizes an indwelling "foreign" object, such as a catheter, mesh, implant.
Since everyone has S. epidermis and other such "benign" Staph, most regular MDs will likely dismiss this, and treat this as normal flora from the front of the nose or skin. And that since 20%+ of people harbor MRSA, finding multi-drug-resistant Staph is no big deal. The trouble with S.epidermis and other coag-neg staph on mucus membranes that most of these can form a biofilm, and may cause low-grade inflammation, secrete toxins, and trade resistance genes with other species of Staph (such as S. Aureus).
 
Dr. Shoemaker is a fringe doctor, not an utter crackpot, but .... he has interesting theories and protocols, but NOT not rigorous studies, no pathology/immunology collaborators, no clinical trials. He is revered in some circles, and reviled by many. Years ago he found mold in buildings as a source of chronic illness. Now he's got a complex protocol for chronic disease that starts with eradicating mold, and includes a bunch of other steps to get at these persistent infections, methylation issues, etc. (I may have it a bit wrong; it's been a few months since I looked him up). (Note: There was a lawsuit against him, which he lost, and was forced to retire from active practice so now he has a company instead. The problem is that there have been no clinical trials of his protocols, nor even carefully done case series to substantiate his theories, e.g., that that nasal MarCONS are associated with marks of inflammation, BBB break-down (even in rats), etc.... I take his pronouncements with a mound of salt. I don't dismiss all he said. But I try to find well-done studies that back what he writes.
 
What convinced me that MarCONS are worth treating were two studies. First, a 2010 publication showing that S. epidermis (normally considered to not produce toxins, unlike S Aureus), actually does produce a potent toxin against leukocytes, just not in as large an amount.
 
And, second, a more damming article: A study of 30 tissue samples removed during surgery for chronic sinusitis, in which 97% had bacteria, and 23 of 30 had biofilms.
37% of different strains found were those of Coag-neg S. epidermis.(The next biggest variety was of, E. Coli with 10% of the 62 strains. Of the 62, 58 strains were cultured, and "only" 29% strains were biofilm forming strains. However, 23 of 30 of the deep nasal mucosal samples showed biofilm formation, with destruction of the epithelium, ranging from disarrayed to absent cilia. (Scanning electron microscopes were needed to identify biofilms, which is why that's not a normal test ).
 
So, if the MarCoNS are only found on a 3-week culture, they must be slow-growing, and slow-growing staph are often ones enveloped within biofilms, hidden from the body's immune system or antibiotics, but able to release toxins to make their homes more hospitable. That is the logic.
 
Lastly, for anyone who wants to go deeper into the effects on local immunity and activation/inflammation, and on the complexity of "what causes" chronic sinusitis,
 
PLoS One. 2015 Aug 14;10(8):e0136068. doi: 10.1371/journal.pone.0136068. eCollection 2015. Association of Mucosal Organisms with Patterns of Inflammation in Chronic Rhinosinusitis. Chalermwatanachai T1, Zhang N2, Holtappels G2, Bachert C3. Their conclusion is that it is not any particular set of bacteria, but likely "dysbiosis", an imbalance of the normal set of bacteria that results in an overgrowth of one or a few types, [and thi density is what allows there to be enough to initiate a biofilm]. Which suggests that even a powerful spray like BEG may only be a part of the solution; that one also needs to re-establish a good broad microbiome. But how?? I don't know.  
Am J Rhinol Allergy. 2012 Mar-Apr;26(2):104-9. doi: 10.2500/ajra.2012.26.3718. Epub 2011 Dec 16. Biofilm formation and Toll-like receptor 2, Toll-like receptor 4, and NF-kappaB expression in sinus tissues of patients with chronic rhinosinusitis. 
Laryngoscope. 2013 Oct;123(10):2347-59. doi: 10.1002/lary.24066. Epub 2013 Apr 1.
Use of topical nasal therapies in the management of chronic rhinosinusitis. Wei CC1, Adappa ND, Cohen NA.

Here's the link to the paper https://www.jci.org/articles/view/80792/version/1/pdf/render
and a summary
 
Researchers have discovered how immune cells triggered by recurrent Strep A infections enter the brain, cause inflammation, and may lead to autoimmune neuropsychiatric disorders in children, including PANDAS. Children with PANDAS exhibit high levels of anxiety, motor and vocal tics, obsessive-compulsive behaviors and a host of other symptoms that often appear “out of the blue” or increase dramatically, seemingly overnight.Their study found that immune cells reach the brain by traveling along neurons that originate from the nasal cavity.
 
This study explains, for the first time, exactly how upper respiratory infections can trigger both physical and neuropsychiatric symptoms.
 
According to the study’s co-leader, Dritan Agalliu, PhD, at Columbia University Medical Center, the Strep A bacterial cell wall contains molecules similar to those found in human heart, kidney, or brain tissue. These “mimicking” molecules are recognized by the immune system, which responds by producing protective antibodies. But because of this molecular mimicry, the antibodies react not only to the bacteria but also to the body’s own tissues. The molecular mimicry process has been well researched by others. But previously, scientists didn’t understand how these autoantibodies would gain access to the brain, because brain vessels form an extremely tight blood-brain barrier. This study answers that question.
 
Researches have known that recurrent Strep A infections trigger the production of immune cells known as Th17 cells, a type of helper T cell, in the nasal cavity. But it was unclear how these Th17 cells lead to brain inflammation and symptoms such as those seen in children with PANDAS. Through this study, Drs. Agalliu and colleagues found that bacterial-specific Th17 cells move along the surface of olfactory, or odor-sensing, axons that extend from the nasal cavity through the cribriform plate, a sieve-like bone that separates the nasal cavity from the brain. From there, the cells reach the olfactory bulb in the brain, which processes information about odors. The Th17 cells break down the blood-brain barrier and enter the brain,, allowing autoantibodies and additional Th17 cells to enter the brain, causing neuroinflammation.

In addition to illustrating how PANDAS occurs, the study also validated some of the experiences many parents have had regarding their PANDAS children:
Strep A is not the only trigger – Parents have often reported that infections other than Strep A seem to trigger PANDAS symptoms. This feedback was so abundant that researchers proposed making PANDAS a sub-set of a new, larger category called PANS – Pediatric Acute Onset Neuropsychiatric Syndrome. Unlike PANDAS, PANS does not associate the onset of symptoms specifically to a Strep A infection. Dr. Agalliu’s study shows that Th17 cells persist in the brain for at least 56 days after initial infection, even when nasal tissues no longer show signs of an active infection. “Several other bacterial and viral pathogens, including influenza virus, mycoplasma and Staphylococcus aureus (nasal staph infections) induce robust Th17 responses and could also play a role in an exacerbation of behavioral symptoms in children with PANDAS if autoantibody levels are primed by previous (Strep A) infections.” (pg 11 of article).