posted
I went to a neurologist this week (not a LLMD) for testing to see if I have permanent damage from the lyme. No permanent damage was found or any other disease from all the blood work. I have been on atibiotics for lyme and seeing a LLMD for 4 years now and the lingering nuero stuff just won't get better. The neuro doctor wants me to take Mestinon to see if my muscles will work better. Mestinon is used for people with myasthenia gravis. "Myasthenia gravis is caused by a defect in the transmission of nerve impluses to muscles. It occurs when normal communication between the nerve and muscle is interrupted at the neuromuscular junction - the place where nerve cells connect with the muscles they control. Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter substance called acetylcholine. Acetylcholine travel through the neuromuscular junction and binds to acetylcholine receptors which are activated and generate a muscle contraction. In myasthernia gravis, antibodies block, alter, or destroy the receptors for acethlcholine at the neuromuscular junction which prevents the muscle contraction from occurring." Has anyone heard of this in relation to lyme disease? Or if anyone has taken Mestinon (perscription, did it help the muscles at all from the lyme disease? Should I be taking it? My LLMD says OK but I am trying to find out if anyone else had this medication prescribed to them and what the outcome was. Please help!
-------------------- Margaret Posts: 103 | From CT | Registered: Feb 2007
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kam
Honored Contributor (10K+ posts)
Member # 3410
posted
There is a MG group. I am sorry but I don't recall how to connect with them.
MG was one of the things that were being considered with me.
I just recall several of the members wondering about lyme and a few had been hospitalized with an infection and took IV abx.
There MG disappeared after that or went into remission.
I also recall that certain abx will make MG worse.
So, it is tricky.
RE: your question. I was not give the MG drug to take so I can't answer that one.
Posts: 15927 | From Became too sick to work or do household chores in 2001. | Registered: Dec 2002
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Here's some quick research on that drug so that you can make an educated decision:
"Mestinon (pyridostigmine bromide) is an orally active cholinesterase inhibitor.
Mestinon inhibits the destruction of acetylcholine by cholinesterase and thereby permits freer transmission of nerve impulses across the neuromuscular junction."
Now if Bb is absolutely dependent (and it is) on choline to make its cell wall and that choline becomes ``not available'' (because acetylcholine is not being broken down), you could be in for a major herx response.
Metabolic acidosis...watch your saliva pH and adjust accordingly. Alkalinize if needed.
This drug is NOT to be given to those who have asthma (likely those with the HLA gene).
``Pyridostigmine has a relatively
short inhibitory action on ChE
compared to organophosphorus inhibitors such as sarin, a nerve agent of concern in the Persian Gulf War.
The *temporary occupation* (carbamylation) of the active site serine of acetylcholinesterase by pyridostigmine can prevent the long-term inactivation (phosphorylation) caused by nerve agents, therefore pyridostigmine was used prophylactically to protect soldiers from possible nerve agent exposures during the Gulf War."
But...
"After returning from the Gulf War, thousands of U.S. military personnel complained of a variety of symptoms, including prolonged fatigue, headaches, muscle and joint pain, sleep disturbances, cognitive difficulties, and others.
In order to be effective, pyridostigmine was given to soldiers at ***relatively high dosages*** (i.e., sufficient to cause significant ChE inhibition).
While pyridostigmine had been used safely for decades in the treatment of patients with myasthenia gravis, it could have different actions in persons without this disorder. Furthermore, a number of studies have suggested that certain environmental conditions may alter the neurotoxic effects of pyridostigmine."
"Pyridostigmine, a carbamate cholinesterase (ChE) inhibitor, has been used clinically for decades to treat myasthenia gravis.
Pyridostigmine is a polar chemical at physiological pH (containing a quaternary ammonium group) and therefore should be largely prevented from entry into the central nervous system by the blood-brain barrier.
Generally, anti-ChE effects of pyridostigmine are considered to be limited to the peripheral nervous system ...''
Then why did the soldiers return with neuro symptoms?
(Research TNF alpha and the BBB)
"Another blood treatment, intravenous immunoglobulin therapy, is also used for myasthenic crisis.
In this procedure, large quantities of purified immune proteins (immunoglobulins) are injected. For unknown reasons, this leads to symptomatic improvement in up to 85% of patients. It is also too expensive for long-term treatment."
Serine is not being phosphorylated. This is disrupting the HPA and HPT axis. Bb has a PKC inhibitor which looks to be PKC, delta form. This impacts the CD3 delta T cells.
"As for a connection between ACh and immune responses, Fujino et al. determined that "In this study, we found that muscarinic ACh receptors [G protein-coupled receptors] exist in
both CD4- and CD8-positive lymphocytes
and that activation of the receptors enhances
***TCR/CD3*** (T cell receptor)
complex-induced mRNA expression of IL-2 and IL-2 receptor subunits, production of IL-2, and cell proliferation."
Therefore, interference with ACh signalling could result in immunosuppression."
If the CD3 cells are "damaged" (gamma-*delta*), this messes up the signals to the CD4 T cells.
Bb uses the "extra" phosphate (which should have gone to serine) to do this:
glucose -> fructose via PFK which it is depleting.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
-
Marnie -
thanks so much for being here. Someday I'll be able to actually read your work in one sitting - but - thank God and Goddess for copy, paste and print.
I have a sister-in-law with MG and this may be helpful for her.
And . . . for all of us, too. So many connections to consider.
posted
Almost. I had developed equivocal (borderline) anti-striatal muscle antibodies and had been referred to a neurologist, but I think my acetylcholine antibodies ended up being okay and not consistent with an MG diagnosis. I figured out I had Lyme though, so I never saw the neurologist.
If you're having trouble with 'communications' between nerve cells and muscles though, consider this...
Neurological Effects of Radio Frequency Electromagnetic Radiation Relating to Wireless Communication Technology - Dr. Henry Lai
Blood-Brain Barrier, Cellular Morphology of the Brain, Neural Electrophysiology, Changes in Neurotransmitter Functions, Metabolic Changes in Neural Tissues, Cytogenetic Effects:
This is what is causing my problems, and it's scary to think that, had I not figured it out, my brain could have stopped communicating with my lungs and I would have died of respiratory failure.
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