posted
Here's the story. I happen to know someone who is having symptoms that are similar to Myasthenia Gravis, but so far testing is inconclusive. Her Lyme WB was negative by CDC standards. (see other post below)
Her symptoms come and go (both MG and Lyme)
Difficulty swallowing episodes POTS like tachycardia episodes Muscle weakness as day progresses Strange eye muscle weakness (sees horizontal double vision like the one eye gets stuck to the side) Brain fog
Lupus tests neg, Lyme ELISA negative, Bartonella IGX negative, thyroid slightly elevated at illness onset, EMG normal, autoanibodies for MG were negative, Tilt table had tachycardia but no drop in BP, MRI of spine normal basically. They did find a pineal cyst in brain but said it was benign and wouldn't cause these problems. Also, her ECG showed 1st degree block at onset of tachycardia and POTS like symptoms.
She went to a neuro that specializes in MG but they told her no, you don't have MG but she wasn't symptomatic that day and appt was in the morning. She usually has eye drooping as day goes on.
*** So I did some research about MG and found that it is an autoimmune condition. The body produces enough acetylcholine and the acetylcholine is able to move across the neuromuscular junction but the receptors are damaged or defective and are not able to take up the Acet. So the muscle fatiques and becomes weak.
The condition worsens with stress, thyroid problems, and illness. Some have ocular MG only which is restricted to the eyes.
With MG, there are medications that can make the condition worse and make them go into crisis. This includes ANTIBIOTICS and beta blockers and calcium channel blockers, both of which she was prescribed. MG patients are also advised to NOT take Magnesium.
I know that many people with Lyme have muscle fatigue, drooping eyes, difficulty swallowing, brain fog, tachycardia stuff.
So perhaps with lyme we are able to produce the acetylcholine but it is a problem with the receptors not being able to take it up??
Why are are symptoms so similar but yet treatment is opposite?? IS MG really Lyme or has Lyme turned into MG???
posted
So here is her WB from IGX. This was taken about one month into symtoms.
IGM 23-25 IND 31 IND 39 IND 41 + 66 + IGG 39 IND 41 ++
She was clinically diagnosed by LLMD and started treatment. She took doxy, a 2 weeks of ceftin and just a short course (like a week or 2) of zithromax and then quit "because she was getting worse".
She never went back to the LLMD and has continued to get worse since being off of antibiotics. Both she and her primary internsist do not think she had lyme. She thinks that antibiotics are bad for her because she 'might' have MG.
Some of her other symptoms in addition to what I listed in the first post are paresthesias on one side of body and on scalp, joint pain, depression, and Raynauds.
She gets very angry when I mention the possibility of possible Lyme and says "EVERYBODY has a positive 41" and "I don't have Lyme!" I hate to see her suffer.
If she really does not have lyme is sure is a weird coincidence that she has POTS and all of these Lyme like symptoms with Myasthenia gravis. I haven't found info anywhere where people with Myasthenia also have paresthesias and joint pain, except for those (<2%) than also have Rheumatoid arthristis with MG.
I hate to see her suffer like this and worry that she possibly has undertreated lyme and it is only getting worse.
If it is MG, she needs to get on some Mestinon or something because they aren't doing anything for her!!
-------------------- Some day, this mamma's gonna dance! Posts: 199 | From here | Registered: Apr 2005
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
I don't like antibody testing.
We are not looking for the pathogen, but instead our reaction TO the pathogen.
I suspect "damaged" antibodies aren't "counted".
And believe me, in lyme there are MANY damaged antibodies.
Hope you understand the following, but if not, let me know and I will try to translate.
(Incidentally our antibodies look sorta like stalks of broccoli and the fab portion is at the top.)
Our own antibodies are not "perfect" fighters against Bb, why?
Characterization of the physiological requirements for the bactericidal effects of a monoclonal antibody to OspB of Borrelia burgdorferi by confocal microscopy.
The bactericidal effect of Fab-CB2 is not dependent on the induction of spirochetal proteases but
is dependent on the presence of Ca2+ and Mg2+.
Supplementation of Ca2(+)- and Mg2(+)-free medium with these cations
restored the bactericidal effects of Fab-CB2.
The mechanism by which a Fab fragment of an antibody destroys a bacterium directly may represent a novel form of antibody-organism interaction.
PMID: 9125579
A ``novel form of antibody-organism interaction?'' I don't THINK so!
E. Required by immunological process. Magnesium, immunity, and allergy: Mg is required for several steps of immunological reactions
1. Lymphoblastic transformation, a prerequisite of secretion of antibodies by lymphoblasts, requires Ca2+ and Mg2+
2. Mg is required for synthesis of proteins, immunoglobulins included
3. Antibody-induced complement activation is Mg dependent
4. The antigen-immunoglobulin-complement reaction induces degranulation of the mastocyte
She did not test positive for the autoantibodies for Myasthenia, but like in lyme, there can be false negative. Here symptoms resemble both Lyme and Myasthenia G.
I understand the importance of Mag with Lyme. I take it myself.
The Dilemma - WHAT does she have??
Lyme= take magnesium, supplement the immune system, take antibiotics, etc.
Myasthenia Gravis (MG) = NO Magnesium, No antibiotics, downregulate the immune system with steroids, immunosuppresives, thymectomy, etc
ARRGGH!!
-------------------- Some day, this mamma's gonna dance! Posts: 199 | From here | Registered: Apr 2005
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
My thought too...remove the thymus for both of these diseases?
(Would need low level cortisone the rest of one's life.)
What pathogen would trigger MG? And why is it usually later in life?
One that uses N-acetyltransferase? Since melatonin production usually declines in later life anyway. Bb uses C-acetyltransferase to stimulate us to MAKE acetylcholine.
Some explanations:
ACh = acetylcholine
AChR = acetylcholine receptor
acetylcholinesterase = enzyme needed to break down acetylcholine when it has completed its job
posted
Thanks for the link, i will check that out.
This is a relative of mine. She just turned 28. There actually are some forms of congenital Myasthenia Gravis as well.
I did also read that some with seronegative (AChR Ab neg) may in turn be Ab postivie for muscle specific tyrosine kinase (MuSK MG) antibodies. I think she was only checked for AChR antibodies so I will have her ask her doc about MuSK antibodies. These people have more muscle wasting and she does have a lot of wasting now.
Again, I still can't help but look at the Lyme WB and those very Bb specific Indeterminates.
-------------------- Some day, this mamma's gonna dance! Posts: 199 | From here | Registered: Apr 2005
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