Dr. Fallon said he was looking at IVIG for Lyme treatment, myasthenia can also be treated (for short-term) with IVIG. (According to wikipedia.)
I wonder if he has had any luck (even short-term), and if we should really be looking at acetylcholine or neurotransmitter receptor autoimmune actions a specific lyme antibody or antibodies may have.
Please tell me if anyone has any more details on this, if they exist. Thanks.
(MG seems to focus on the nicotinic acetylcholine receptor antibodies, rather than M1 muscarinic, but i wonder how different the receptor antibodies are. Would certain tests cross react? Could the case report be showing a cross-reaction of acetylcholine receptor antibodies of different types?)
Posts: 244 | From Ottawa | Registered: Dec 2005
| IP: Logged |
posted
this could also explain "post-lyme" if it exists, and if it isn't caused by remaining lyme bacteria in the sufferer.
the spirochetes could really die, but their antibodies may remain in the body and replicate for a very long time (very likely potentially forever depending on individual immune systems), much like vaccines do, and it could be them that are causing the lasting ill effects. this would theorize that chornic lyme may be an autoimmune disease.
theoretically, response to long-term antibiotics in some people may be an illusion, if that just says how long it took for the antibodies to clear their system. or if they experiencing benefits secondary to a certain drugs antibiotic activity, and many antibiotics have cryptic effects elsewhere, including the nervous system, where some have been theorized to have therapeutic capacity beyond and unrelated to antibiotic effects, as has been discussed here, i think.
or it could easily be a combination, i.e. active lyme infection, autoimmune effects, or both.
Posts: 244 | From Ottawa | Registered: Dec 2005
| IP: Logged |
posted
Active Lyme infection, autoimmune effects, or both.
I vote for both. This is thought-provoking, daniel. With Lyme, since our immune system doesn't have the capacity to get rid of the infection, it goes for whatever it knows how to fight, even if it's really wrong and causes even worse problems than the persistance of the microbes.
Autoimmune disease has to have a trigger. How to safely stop the process, whether or not there is an infection, is the challenge!
Having antibodies to "muscarinic acetylcholine receptors" sounds like it could cause some bad nerve juju.
Posts: 353 | From Florida boonies | Registered: Nov 2005
| IP: Logged |
Hubby has been tested one or two times at least for myasthenia gravis. He has a ptosis (droopy eyelid) which is often a subtle sign of that disease. Can't remember offhand exactly what test was done for myasthenia gravis.
Hubby has on and off-again tremors/myoclonus and seizure-like episodes. There is definitely a cholinergic connection to his neuro symptoms.
In the past IV phosphatidylcholine (to INCREASE choline) greatly decreased tremors etc (P.K. protocol). Currently IV phenergan (for nausea) works better than IV Ativan for tremors etc -- this med is mildly anticholinergic (DECREASES choline). Unfortunately the symptoms of too much or too little choline are identical -- tremors and movement problems etc.
Then there is the Babesia factor to consider. Babesia uses phosphatidylcholine as does Lyme.
Bea Seibert
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
| IP: Logged |
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
Printer-friendly view of this topic