LNN

Elizabeth, Are you looking at KPU because of treatment relapse or some other reason? Thanks for the article link - very helpful. Getting zinc/copper et al tested this week as part of a blood draw to check on liver function. My antenna is now really up on all this stuff. Its like pulling on a loose thread. You find it's attached to so much other stuff and sometimes I feel like I'm on dance step #4, thinking we're making progress, only to find we need to take steps backward and start at an earlier step. It would be one thing if we were dealing with an adult. But with kids, they're forming their identities, missing key steps in building an academic foundation, while we flop around, trying to figure this out before they lose even more time. I think it's this sense of lost childhood that is the hardest thing for me to deal with. Laura

Can you share what brand you're using? Did you come across any pill forms that would be good options? I'm already looking at having to get a drink into him with fiber/miralax to prevent constipation/encourage BMs, so don't see much success in having to get multiple "disguised" drinks into him. I see NOW Foods has a 1000mg chlorella tablet - that might be an option. Any input? Justine - Yes, also read bad stuff about Actos - things that made me discount it as an option for us. But now I can't find it again.

Yes - what took me 3000 words = you summed up in 4 sentences! You get it! I too wondered why DS did so great on month-long prednisone tapers. Like your girls, it was a miracle for him. Which is why I dismissed lyme for so long. But now I think that if this is true for DS, then the lyme lowers MSH, sets off a cytokine storm, genetic susceptibility results in poor detox/autoimmunity/immune dysfunction, and the inflammation in the basal ganglia interrupts normal signalling and results in neuropsych symptoms. Prednisone would halt to cytokine storm (but chronic lyme would set the whole thing back in motion which could explain our inability to sustain remission longer than 2 months (vs. the strep "exposure" theory I once thought). Shoemaker advocates using binding agents in a big way as part of the regular lyme treatments. He likes Actos (a diabetes drug) + Cholestryamine (a cholesterol drug that works by binding) but don't think either are appropriate for kids. And for the record - yes, I woke up at 3am on Wed due to stress and worry. But then Thur night was woken by DS who had lost his blanket (and felt I should be awake to know this) and last night by DD who also felt I needed to know she was cold and uncovered. Once I get fully woken, it's hard for me to get back to sleep. But I'm not quite as stressed as I sounded. Tonight I will duct tape the blankets to their shoulders and hopefully sleep well. Got 10 charcoal pills into DS without issue today. Isn't practical during school days, but will be putting together a serious plan for the summer. I think DS feels so bad right now that he'll cooperate (at least until he starts to feel better).

The short answer is that you find the strength because you have no other choice. But there are things you can do to help. First, having a doctor(s) who supports you is critical. It takes away a lot of the anxiety that comes with feeling like the survival of your family, your marriage and your child's health sits solely on your shoulders. However, having been at this for way too long, I can tell you that you never get to hand over the car keys and let any doctor take over completely. We too have found that doctors who follow a more integrative approach have been able to help us more. But the days of being able to let someone else be the case manager are over, regardless of their approach. You have a new job from which you cannot resign. Second, having a support system is equally critical. The rate of divorce is high in the general population. I imagine it's even higher in families that struggle with health and mental health issues. You cannot do this alone and you should try as much as possible to bring your family and your support group along with you as you discover, process and adapt. Otherwise, it's really really hard to stay on the same page with the rest of the world. Third, this disease will permanently change how you view life, but you can't let it become your sole identity. You have a child with Pandas, but your child continues to be so much more than Pandas. Don't lose sight of the big part of him or her that has nothing to do with illness. I think one reason some people leave the forum is that you need to move beyond cyber world and live life. This forum has a role - to educate, to support, to explore ideas. But you still need to nurture all the aspects of your life you had before this happened. At this point in your journey, this probably seems impossible. But always keep it as a goal. It's good that people move on. No offense to any of the friends I've made here, but I can't wait for the time that checking the forums becomes a distant memory. What you're going thru is an evolution. Big growth doesn't come painlessly. Keep learning as much as you can. Question everything. Try not to become married to any one idea or solution. I don't think there's one "cure" - no holy grail at this point. But I do think there are individual answers, things that work for individual kids. Your job is to find that unique answer for your own child. Could be strep, could be mycoplasma, could be lyme, could be something else. At times, it feels like time is the enemy, that you have to figure this all out NOW and there needs to be ONE answer. It may not be that simple. But try not to lose yourself or the rest of the family in the process of discovery. It's a balancing act. But you can do it.

What does milk thistle do? This does a decent explanation http://books.google.com/books?id=J4TFtQeHkQAC&pg=PA174&dq=milk+thistle+lyme&hl=en&ei=74XXTce2BefX0QGDg_D7Aw&sa=X&oi=book_result&ct=result&resnum=1&ved=0CEMQ6AEwAA#v=onepage&q=milk%20thistle%20lyme&f=false Milk thistle is a liver detox. It helped DS and I started taking it and feel much better. I'm in good health overall but there's just a wee bit of stress that comes with raising our kids and this seems to help me feel clearer, more energy, more "on my game".

I've been researching MSH (melanocyte stimulating hormone) a lot this week. This is a hormone that controls inflammation and in lyme patients tends to be seriously low. For the past 2 months, after changing abx and adding tindamax, DS has been very Pandas-like. Return of tics, handwriting looks like a stroke victim, mood issues, yada yada. We stopped tindamax a few weeks ago and things have been tapering down. But this week, I got a call from the teacher saying DS was acting inappropriately, unable to regulate behavior, unresponsive to discipline, not hearing his name when called repeatedly. At nights, he wasn't all there. He was like a Stepford wife - sort of muted and dull, on autopilot, mentally someplace far away. So I get out the motrin and see an immediate improvement. Teacher tells me yesterday he was significantly better. So I'm thinking we're really in a bad spot. If treating lyme puts him into a Pandas state, we can't use the tools to beat lyme and since he has lyme, we can't use the Pandas tools like prednisone to stop the cytokine storms. So I've been awake at 3 am most of this week, chasing down our recent forum topics on MSH and the HLA gene. Then I found this: http://www.publichealthalert.org/Articles/scottforsgren/biotoxin%20pathway.html It is important that we look deeper in terms of recognizing that there may be more than just an infection with Lyme disease or an exposure to mold at the core of one’s ongoing symptom picture. Biotoxins, and the inflammatory responses which they initiate, may be at the center of the illness. If a person is genetically susceptible to a biotoxin-associated illness, it is likely the case that the biotoxins themselves, rather than Lyme infection or mold exposure, are causing many of the symptoms being experienced. Even further, it is plausible to suggest that infection could be cleared, or the exposure entirely removed, and yet the remaining symptoms may be almost entirely due to circulating biotoxins. It comes down to a genetic predisposition which results in the body’s inability to remove these biotoxins. Long after the initial exposure or infection is gone, the toxins may live on.... There are specific genotypes associated with specific susceptibility to biotoxins. For patients with Lyme disease or mold exposure, approximately 25% of the population has a genetic predisposition which results in an inability to clear biotoxins naturally. Understanding whether or not one is in this population can provide key insight into the cause of illness. Though the result may suggest a genetic make-up which cannot itself be corrected, once known, specific interventions can be put into play that may significantly improve the outcome. The test is called HLA DR and it is commonly known as a test which provides insight into possible organ rejection after a transplant operation. Human Leukocyte Antigen (HLA) is a grouping of genes that lie on chromosome 6. In the case of biotoxins, HLA codes for whether or not a person is capable of clearing biotoxic substances following an exposure. For these people that are genetically incapable of clearing these toxic substances, biotoxins will continue to circulate within the body indefinitely and may reduce one’s chances of recovery. There is generally no “selfhealing” in these cases without appropriate interventions. The “Biotoxin Pathway” illustrates an ongoing, amplifying cascade of events that starts with exposure to a biotoxin in those individuals who are genetically susceptible. The biotoxin then binds to Toll receptors, primarily in fat-cells and cells that line blood vessels, resulting in the production of proteins called cytokines which are involved in immune response and inflammatory processes. Cytokines recognize invaders and recruit additional cytokines in response. In the world of biotoxins, it is the biotoxin itself that continuously signals the body to produce more cytokines. It is this excess cytokine production that makes us feel unwell. Excess cytokines result in flu-like symptoms, body aches, temperature fluctuations, cognitive difficulties and other symptoms. This increase in cytokines has further downstream effects. VEGF (vascular endothelial growth factor) is often reduced which leads to fatigue and reduced blood flow. Hypoperfusion, this resulting reduction in blood flow, results in a starving of cells for nutrients and oxygen. There is also an increase in MMP9 (matrix metalloproteinase) as the cytokine itself causes the white blood cells to release MMP9. MMP9 is a superb marker for the presence of excess cytokines. MMP9 may be responsible for delivering inflammatory compounds out of the blood and into the brain which causes plaque formations similar to those seen in MS. In Lyme disease, MMP9 levels may skyrocket as the result of treatment with antibiotics and the resulting bacterial die-off in what is commonly referred to as a Herxheimer reaction. Taking this even further, if you give a Lyme-infected person antibiotics and they are not HLA-susceptible, they generally have an uneventful recovery. An increase in cytokines may also trigger auto-immunity. There are three key types of antibodies observed in those with biotoxin-associated illnesses. These are myelin (the protective sheath around nerve cells) antibodies, gliadin (a protein found in gluten) antibodies, and cardiolipin antibodies which impact circulation in the small blood vessels. There may be notable increases in markers which reflect activation of the complement system, namely in C3a and C4a. There is a significant difference in C3a and C4a levels between controls and the Lyme or mold population. In fact, C4a levels invariably become elevated, often as early as twelve hours after a tick bite. In the case of those with a mold-susceptible HLA type, C4a significantly increases within four hours after re-exposure to a moldy environment. C4a can be a helpful marker in determining whether or not a remediated home is still a danger for someone with mold biotoxin susceptibility. If C4a levels have been reduced via appropriate interventions and C4a levels rise upon reintroduction to the suspect environment, it is a sure sign that the environment is not safe for the patient. MSH, which is made in the hypothalamus, is the most potent anti-inflammatory compound we have. It is responsible for regulating innate immune response and is involved in numerous hormone pathways. Reduced MSH is at the heart of the “Biotoxin Pathway” in that many negative downstream effects result when MSH is low. Of interest here is that in Lyme disease, chronic fatigue syndrome, mold illness and any other biotoxin illness regardless of the source of the biotoxin, MSH is low in about 95-98% of patients. When MSH levels are low, people become sleep disturbed; they have chronic pain; they experience leaky gut syndrome; their recovery from illness is delayed; they develop multiple antibiotic resistant coagulase negative staph colonization (MARCoNS); they have frequent thirst as a result of lowered anti-diuretic hormone (ADH); they have a loss of libido due to a lowering of sex hormones and more. MSH is involved in the production of melatonin and endorphins. This resulting lack of endorphins increases our perception of pain. MSH regulates the protective cytokine responses in the blood, skin, digestive tract, and respiratory membranes. Lowered MSH results in abnormalities in production of cortisol and fluctuations in ACTH (adrenocorticotropic hormone) which regulates adrenal function. It is when the biotoxin illness disrupts the production of MSH that so many of the symptoms begin to appear. When looking at the results of lab tests for reduced MSH and increased C4a, the difference between patients and controls is clear. Using these markers, the diagnostic accuracy of the Shoemaker model is compelling. These are only excerpts. I cherry-picked paragraphs. The article goes on to discuss treatments, but geared toward adults. But I feel like I finally found the missing puzzle piece of why we do everything we're "supposed to" do and yet my son stays sick. This is beyond "herx" in the traditional sense. It's a chain reaction. We'll hopefully get the lab reqs to test MSH and HLA in the next week (must be done at Labcorp). I know a few others are in the same boat...maybe this will help all of us.

Under Helpful threads, there are links to some articles that may help. None of the lyme labs are foolproof - lots of reasons why. But as Michael said, Igenex is "better" than a standard lab using CDC criteria because some of the antibodies they look for are lyme specific (31, 39) and CDC western blots intentionally don't look for these due to the horribly out of date reasoning that the lyme vaccine would cause healthy people to test positive. The vaccine was a total failure and was pulled off the market after only 2 yrs in 2002(?). Many believe that if you test positive for 31 or 39, it doesn't matter how many other bands are positive. You probably have lyme. The lyme path is no easier than Pandas. The "cure" is just as elusive, expensive and gut wrenching. Like Pandas, you have to learn as much as you can, sort thru hypotheses and conventional wisdom and misinformation and trust your gut. Like Pandas, all the theories in the world only take you so far. The proof is in the pudding. When they get well, you've found your answers - for either disease. In the meantime, you post on forums

I'm between LLMD appts and reviewing the cupboard to see what we're low on. I got to wondering, as I stood awestruck at how many pills I ask my kids to pop each day, just how "essential" each one is to their recovery. I know Milk Thistle has made a significant difference - saw changes immediately - and I started taking it myself - and I can tell when I've skipped a day or two. On the other hand, we dropped ALA in favor of glutathione because DS didn't think the ALA did all that much. So I'm asking for opinions... With the goal of minimizing the number of daily pills - including abx - and of keeping costs as reasonable as possible, what supplements do you consider "essential", "helpful but not essential", or "not sure it does much". With 5-7 abx pills in the mix, my goal is to use no more than 5-6 additional pills per day. Here's my list: Essential: 1. probiotics (using 1 Theralac 30 Bill CFUs with 1 TruFlora for yeast 2x/week) 2. multivitamin (alternate between Juice+ and generic multi) 3. milk thistle 4/ Trufiber and/or miralax (for drainage - my kids don't eat well enough to keep the pipes moving frequently enough for detox purposes) Helpful but...: 1. Glutathione (try to take on empty stomach but not always possible on busy school mornings) 2. Motrin (use when Pandas-like stuff impacts the family) 3. Quercetin (mostly for temp. allergy relief, not for lyme or Pandas per se - find motrin more effective for inflammation behaviors) Not sure it does much: 1. Tumeric 2. ALA (switched to glutathione) 3. Activated Charcoal - probably not effective b/c only giving 3-4 pills but can't see asking him to swallow more every day, and liquid clay isn't an option - no way it's getting swallowed. 4. Fish oil Your opinions? Please feel free to add homeopathics, naturals etc, but if it's a liquid, please let me know. Pills are far easier to get into my kids than something they can taste. I'm shooting for practical and affordable, biggest bang for the buck.

We had good results with a bactrim+zith+augmentin combo. But I also think regular 'ol lyme is at play, so we dropped the augmentin and added omnicef two months ago. But DS has, so far, responded to oral abx, so I'm not sure I can suggest anything, since your son has been treatment resistant to orals. You may want to ask for additional input on www.lymenet.org as they have tons of members with a wide array of experiences. We are not out of the woods, so my experiences may not be very helpful.

For anyone in the area, Dr J and Dr Burrascano will be presenting at a symposium this Sat. http://www.newhaven.edu/unh/lyme/index.html

Is your son taking the cholestyramine or just you? Wasn't sure if kids could use it.

Two kids at $5k? The quotes I got for one child is not near that. Your lucky. Georgetown's bills came to about $23K for us (3 days in PICU). Insurance negotiated rates dropped it to $18K (I think - it was 2 yrs ago). But we had met our deductible and only had to pay 20%, so our out of pocket was about $3600, plus $1800 in travel, hotel, etc since we had to take the whole family to DC (no extended family to help out). So $5500 - roughly what we had to pay for IVIG as well. (this kid better take care of us when we're old!) Pex was a good experience for us but it wasn't sustainable. And it long before we ever considered lyme. As a general theory, I tend to agree with Kim, but I can also understand being at a point where relief can be priceless, even if it's temporary. I think the hardest part for us was that the word "cure" was used, so the steps backward, when they came, were heartbreaking. You'll have all of our support no matter what you decide. Unfortunately, as always, you have to trust your own gut.

Did the knowledge that your MSH levels were low alter your treatment plan? In other words, if I ask LLMD to measure it, does it change what we do/take, or is it just more data to make me feel better about the course we're already on?

Just saw this NTY article... Control Desk for the Neural Switchboard By CARL E. SCHOONOVER and ABBY RABINOWITZ Treating anxiety no longer requires years of pills or psychotherapy. At least, not for a certain set of bioengineered mice. In a study recently published in the journal Nature, a team of neuroscientists turned these high-strung prey into bold explorers with the flip of a switch. The group, led by Dr. Karl Deisseroth, a psychiatrist and researcher at Stanford, employed an emerging technology called optogenetics to control electrical activity in a few carefully selected neurons. First they engineered these neurons to be sensitive to light. Then, using implanted optical fibers, they flashed blue light on a specific neural pathway in the amygdala, a brain region involved in processing emotions. And the mice, which had been keeping to the sides of their enclosure, scampered freely across an open space. While such tools are very far from being used or even tested in humans, scientists say optogenetics research is exciting because it gives them extraordinary control over specific brain circuits — and with it, new insights into an array of disorders, among them anxiety and Parkinson’s disease. Mice are very different from humans, as Dr. Deisseroth (pronounced DICE-er-roth) acknowledged. But he added that because “the mammalian brain has striking commonalities across species,” the findings might lead to a better understanding of the neural mechanisms of human anxiety. David Barlow, founder of the Center for Anxiety and Related Disorders at Boston University, cautions against pushing the analogy too far: “I am sure the investigators would agree that these complex syndromes can’t be reduced to the firing of a single small neural circuit without considering other important brain circuits, including those involved in thinking and appraisal.” But a deeper insight is suggested by a follow-up experiment in which Dr. Deisseroth’s team directed their light beam just a little more broadly, activating more pathways in the amygdala. This erased the effect entirely, leaving the mouse as skittish as ever. This implies that current drug treatments, which are far less specific and often cause side effects, could also in part be working against themselves. David Anderson, a professor of biology at the California Institute of Technology who also does research using optogenetics, compares the drugs’ effects to a sloppy oil change. If you dump a gallon of oil over your car’s engine, some of it will dribble into the right place, but a lot of it will end up doing more harm than good. “Psychiatric disorders are probably not due only to chemical imbalances in the brain,” Dr. Anderson said. “It’s more than just a giant bag of serotonin or dopamine whose concentrations sometimes are too low or too high. Rather, they likely involve disorders of specific circuits within specific brain regions.” So optogenetics, which can focus on individual circuits with exceptional precision, may hold promise for psychiatric treatment. But Dr. Deisseroth and others caution that it will be years before these tools are used on humans, if ever. For one, the procedure involves bioengineering that most people would think twice about. First, biologists identify an “opsin,” a protein found in photosensitive organisms like pond scum that allows them to detect light. Next, they fish out the opsin’s gene and insert it into a neuron within the brain, using viruses that have been engineered to be harmless —“disposable molecular syringes,” as Dr. Anderson calls them. There, the opsin DNA becomes part of the cell’s genetic material, and the resulting opsin proteins conduct electric currents — the language of the brain — when they are exposed to light. (Some opsins, like channelrhodopsin, which responds to blue light, activate neurons; others, like halorhodopsin, activated by yellow light, silence them.) Finally, researchers delicately thread thin optical fibers down through layers of nervous tissue and deliver light to just the right spot. Thanks to optogenetics, neuroscientists can go beyond observing correlations between the activity of neurons and an animal’s behavior; by turning particular neurons on or off at will, they can prove that those neurons actually govern the behavior. “Sometimes before I give talks, people will ask me about my ‘imaging’ tools,” said Dr. Deisseroth, 39, a practicing psychiatrist whose dissatisfaction with current treatments led him to form a research laboratory in 2004 to develop and apply optogenetic technology. “I say: ‘Interestingly, it’s the complete opposite of imaging, which is observational. We’re not using light to observe events. We’re sending light in to cause events.’ ” In early experiments, scientists showed that they could make worms stop wiggling and drive mice around in manic circles as if by remote control. Now that the technique has earned its stripes, laboratories around the world are using it to better understand how the nervous system works, and to study problems including chronic pain, Parkinson’s disease and retinal degeneration. Some of the insights gained from these experiments in the lab are already inching their way to the clinic. Dr. Amit Etkin, a Stanford psychiatrist and researcher who collaborates with Dr. Deisseroth, is trying to translate the findings about anxiety in rodents to improve human therapy with existing tools. Using transcranial magnetic stimulation, a technique that is far less specific than optogenetics but has the advantage of being noninvasive, Dr. Etkin seeks to activate the human analog of the amygdala circuitry that reduced anxiety in Dr. Deisseroth’s mice. Dr. Jaimie Henderson, their colleague in the neurosurgery department, has treated more than 600 Parkinson’s patients using a standard procedure called deep brain stimulation. The treatment, which requires implanting metal electrodes in a brain region called the subthalamic nucleus, improves coordination and fine motor control. But it also causes side effects, like involuntary muscle contractions and dizziness, perhaps because turning on electrodes deep inside the brain also activates extraneous circuits. “If we could find a way to just activate the circuits that provide therapeutic benefit without the ones that cause side effects, that would obviously be very helpful,” Dr. Henderson said. Moreover, as with any invasive brain surgery, implanting electrodes carries the risk of infection and life-threatening hemorrhage. What if you could stimulate the brain’s surface instead? A new theory of how deep brain stimulation affects Parkinson’s symptoms, based on optogenetics work in rodents, suggests that this might succeed. Dr. Henderson has recently begun clinical tests in human patients, and hopes that this approach may also treat other problems associated with Parkinson’s, like speech disorders. In the building next door, Krishna V. Shenoy, a neuroscience researcher, is bringing optogenetics to work on primates. Extending the success of a similar effort by an M.I.T. group led by Robert Desimone and Edward S. Boyden, he recently inserted opsins into the brains of rhesus monkeys. They experienced no ill effects from the viruses or the optical fibers, and the team was able to control selected neurons using light. Dr. Shenoy, who is part of an international effort financed by the Defense Advanced Research Projects Agency, says optogenetics has promise for new devices that could eventually help treat traumatic brain injury and equip wounded veterans with neural prostheses. “Current systems can move a prosthetic arm to a cup, but without an artificial sense of touch it’s very difficult to pick it up without either dropping or crushing it,” he said. “By feeding information from sensors on the prosthetic fingertips directly back into the brain using optogenetics, one could in principle provide a high-fidelity artificial sense of touch.” Some researchers are already imagining how optogenetics-based treatments could be used directly on people if the biomedical challenge of safely delivering novel genes to patients can be overcome. Dr. Boyden, who participated in the early development of optogenetics, runs a laboratory dedicated to creating and disseminating ever more powerful tools. He pointed out that light, unlike drugs and electrodes, can switch neurons off — or as he put it, “shut an entire circuit down.” And shutting down overexcitable circuits is just what you’d want to do to an epileptic brain. “If you want to turn off a brain circuit and the alternative is surgical removal of a brain region, optical fiber implants might seem preferable,” Dr. Boyden said. Several labs are working on the problem, even if actual applications still seem far off. For Dr. Deisseroth, who treats patients with autism and depression, optogenetics offers a more immediate promise: easing the stigma faced by people with mental illness, whose appearance of physical health can cause incomprehension from family members, friends and doctors. “Just understanding for us, as a society, that someone who has anxiety has a known or knowable circuitry difference is incredibly valuable,” he said. Here's the link if you want to print it or email it http://www.nytimes.com/2011/05/17/science/17optics.html

But aren't there multiple DR types? On the chart, I see DR(B)1, DR(B)3, 4 and 5. (Don't these doctors realize that we need things spelled out?? )

I'd put much more stock in any answer your doctor could give you, so please ask him/her this same question. However, prior to IVIG, my son's C3d was 51. Two months post-IVIG they were 52 (at that point, DS was in worse shape than pre-IVIG). I asked our Pandas doctor if IVIG shouldn't have made those numbers go lower and was told yes, unless there was still a chronic infection. A month later, we started with lyme treatment. I would still ask your own doctor rather than relying on my hearsay.

I had two thoughts when reading this. The first is that in my own experience, a Pandas flair looks very similar to what we now call lyme. For us, the initial 2 Pandas episodes (with confirmed rapid streps) were far more intense, came with much more severe tics, and (for DS) serious OCD (mild compared to what some of you have dealt with, but worse than we've seen since). Since the last confirmed strep in '08, I'm not sure if what we've called Pandas isn't really TBI. So your DD may or may not be in a "Pandas" flair. If it's lyme-triggered, then you may not see the symptom improvement as quickly with a new abx that you're expecting. It could stay the same or you could even see it worsen (herx). Try to observe and journal (days blur together, as you know). I would give the augmentin some time before asking for something different (2-3 weeks?) Second, if I understand your post, you met with LLMD on Wed, started augmentin Fri and now are scheduled to start tindamax this coming weekend? This is much quicker than the approach we've used. We've been told to wait 2 weeks before adding a second abx, in order to see the reaction to the first one, otherwise, if there was a bad reaction and we started 2 in close proximity, we wouldn't know which once was the likely culprit. So if you're not liking what you see, you may want to ask the LLMD about delaying the tindamax until you at least have a feel for whether things are getting better or worse. Just something to consider.

I'm sure you've seen this if you've already been searching, but just in case... http://www.survivingmold.com/diagnosis/lab-tests I don't know what the numbers mean yet.

Have only just begun to research, but my understanding is that there are multiple HLA gene variants. Two effect your ability to detox/fight lyme, at least one effects your ability to fight mold. One of the HLA variants that is relevant to lyme (don't have the sub-type name handy) is carried by 23-25% of the population and it is this group that was particularly susceptible to adverse reactions from the lyme vaccine that was on the market in 2000-2002 time frame. This group either had lyme and didn't know it or was genetically unable to count a proper immune response to the lyme vaccine and developed rheumatoid arthritis (the manufacturer argued it was unrelated to the vaccine but the potential for law suits from 25% of the population made the vaccine a failure and they pulled it from the market). This is my new research project this week. I'll post what I can find.

Has anyone tested their MSH levels? I find this as a really interesting possible reason for elevated CamK II that we see in Pandas. Aside from Shoemaker, does anyone have research links to this? Very interesting thread...

I asked our LLMD about this at our last visit. We left with a lab req to test magnesium, zinc and copper levels, along with labs to check liver function. Went the other day but was told DS has to be vitamin free for a week first. DS's tics are resolving without added magnesium, but would like to have info in case we need it in the future. Glad you're seeing improvements! (but sorry you're awake at 3am - never a good sign).

Darlene - know how you feel. Thru a strange twist of events, I was able to get an article on Pandas published, at a time when DS was improving, and I wrote how well he was doing, what a great experience pex was...then by the time the article was published in January '10, DS was dealing with another episode (in hindsight, TBI but I thought it must've been from exposure to strep). Later last year, I presented our experiences at two conferences, just prior to and just after IVIG...still firmly believing that we were only dealing with Pandas and that we were still on the right path, just needing a different, aggressive treatment (even tho my best friend had started suggesting I look at lyme). By last fall, I felt pretty embarrassed. Here I was speaking like I had answers but couldn't seem to keep my own son in a good place. There was (and is) still so much I needed to learn. On one hand, you feel the need to go public so maybe others don't have to make the same mistakes you did, but on the other hand, you're not out of the woods and are still following the elephant in the parade, at risk of being pooped on at any time. I'm really sorry you had such a rough time at the doctor's office. I look back and despite the past rough two months, yes, the times in years past were worse. We are making progress. It's just hard to see sometimes. And you have to remind yourself that even 4yos without lyme sometimes mortify their parents in public. (So do 8 yos). Be vigilant, take good notes, then try to let behaviors guide you more than an idea of what "should be" happening. My biggest regret is trying to make all symptoms "fit" into the diagnosis I thought we had and not paying closer attention to what didn't fit. That's why my confidence was rattled these past two months - I don't want to be married to TBIs to the point I miss signs to the contrary. For now, DS has made much more progress with a lyme protocol, particularly academically, so we'll stick with it as long as it helps. But I'm trying to be more balanced this time around. And speaking of "speaking too soon" - I said I normally would've waited longer before posting a positive update but wanted to reassure newcomers. I did see a few tics last night (tho none during the day and none yet today). They are definitely diminishing, but not gone entirely. And Lismom and Wendy - seeing the same emotional lability and a mild case of adhd today. Still far better, but just enough to let you know it's not done yet. Heaven forbid I should get comfortable with the idea of "normal" or "well-adjusted".

That's what I assumed too, but I'm not sure anymore. On Monday two weeks ago (5/2), we stopped omnicef for 4 days. Re-started on Friday (5/6) but didn't do tindamax last weekend (5/6-5/8)(125 mg for 65lb, fri pm, Sat am/pm and Sun am). It wasn't until this Wed (5/11) (10 days after last tindamax and 5 days after our omnicef break) that I saw things definitely calming down. The thinking on doing a weekend pulse is that you'll see herxing on Sat/Sun and maybe Mon/Tue then have a good rest of the week. But I think for my DS, it just wasn't clearing fast enough and we were in perpetual herx between omnicef and tinda. I think we'll stay off tindamax for a few weekends and let DS enjoy the end of school, then re-start in mid-June. When we re-start, I may ask about only doing two doses at start of week (Mon) so that we have a better shot at good family weekends for the summer. Then maybe add in additional doses based on reactions. I think I see that tindamax is certainly needed (DS has been on some sort of abx for 2+ yrs) so I'm sure there's lots of cyst form lyme in there. But the overload of toxins can't be good for the body and certainly isn't good for the rest of the family. So I'm leaning toward a slower course of treatment, trying to find that balance between aggressive enough to stay ahead of reproducing bacteria but gentle enough to stay married and being able to raise a mentally healthy family over the next upteen months of treatment.

A few days ago, I posted about being discouraged, wondering if we were doing the right things, since DS had been struggling for the past 2 months. I was frustrated because this was happening despite 4 abx. So we took 4 days off from omnicef last week - saw no change for 3 days, then a worsening of tics on day 4, so we resumed omnicef. But we skipped tindamax this weekend. I'm happy to say his prolonged struggles may have been because of, not despite, 4 abx. His tics stopped yesterday and his mind was very clear. He felt better than he has since January. So I am back in a comfort zone as far as feeling it's lyme/bartonella and that it was indeed a long herx. When we switched abx in March (dropped augmentin, added omnicef), we saw an immediate worsening (tics for the first time in 18 months). Ok, herx, I thought. Then we added tindamax 2 weeks later (and for two weekends, I mistakenly gave a whole pill for 4 days instead of cutting it in half for each dose). When we hit 7 weeks and things weren't improving, I started to worry. I'm now theorizing that we probably started tindamax too quickly after switching to omnicef and we flooded the system with die-off and the body just wasn't able to detox fast enough. So for anyone new here that I may have spooked, sorry. I generally don't like to post so quickly about improvements, but didn't want my last post to hang out there without the update. To see my son emerge again - no words to describe the relief and happiness. He pulled out a lego robot kit last night and sat at the table building it with my husband. This is something he loves but will only do when he's coming out of an exacerbation - takes concentration and processing skills he doesn't have when he's in an "episode". So it's always like seeing the first robin of springtime when he wants to build things. Think we'll enjoy this for a few weeks then add back some tindamax - but probably at a lower rate. To think that someday, these great days could be the norm instead of the exception...hard to imagine.

Nice job! You don't come off as neurotic at all. But don't you wish they gave it ten pages to talk about so much more, and how hard it was to figure out what was wrong? What gets figured out in one paragraph sums up such a long, exhausting, expensive journey! Glad you're starting a website focused on lyme kids. Considering that kids are one of the largest populations of lyme victims, surprisingly little is out there that talks about their needs and symptoms. I was wondering - while you need facts for the site, not anecdotes, is it worth starting a thread that talks about the things that things our kids experience? And how it's the same or different from other diseases (e.g. Pandas)?