Thanks for clarifying that and jogging my memory. I was going to be a biochemist and still have that leaning, even though I went into the "arts" instead.

First, I wasn't implying that your doc was bad! It was my frustration with neuros in general showing. Sorry. And I never "talk down" to people; I just try to get all the basic info out there - don't want to assume anything.

Well, that's very interesting. If you have too much acetylcholine, you can get the opposite readings of MG. Though the LEMS can be tricky to gauge on an RNS. It temporarily gets better, then dips and then gets better again. But so can SCCMS's. I have to wonder if it showed an increment on your legs because you used them before the test but maybe didn't use your arms!

Fluoxetine is used for slow channel syndrome, as you know. So that is even more curious. Most of the SCCMS's tend to be autosomal dominant, so they are passed down from generation to generation.

I hope they will look for an R-CMAP. Did they see any on the RNS? Maybe they don't know what it looks like since not many people deal with the CMS's. Too bad they don't make copies of the waveforms for patients.

http://books.google.com/books?id=pnn...ntials&f=false

I suppose you could always try drinking some tonic water, which has quinine in it. Though there's not a great amount in tonic water, it might be interesting to try, since it does the opposite of Mestinon. I'm not "recommending" this because if you do have MG, it could make things worse! And I'm not a doctor, so I can't recommend anything.

http://jama.ama-assn.org/content/110/3/198.extract

http://jama.ama-assn.org/content/173/8/932.2

http://www.inchem.org/documents/pims/pharm/pim464.htm

Here's a question. How long do your eyes stay dilated after going to the eye doctor? The eye drops that numb the eye have atropine in them. So, if you had SCCMS, you might feel better. My eyes stay dilated for HOURS afterwards and my MG gets worse.

So heat and cold may make you better if you have SCCMS, which I'm sure you've already thought about. Coffee and nightshades might make you worse.

I'm sorry about your Dad and sister. I too have had lots of those kinds of experiences, unfortunately. You get "educated" very quickly in order to help. It might be useful if they did some genetic tests on your family, once they figure out what is going on for sure.

Since the CMS's are genetic, although they can have adult onset, were there signs of you having issues at younger ages?

I hope you get solid answers. Being in limbo is, at least it was for me, worse than knowing. Thanks for being so honest and putting all of that info out there. I'll bet it will help others.

Annie

http://neuromuscular.wustl.edu/mtime...tml#mgslowchan

MYASTHENIA GRAVIS: ACQUIRED SLOW CHANNEL SYNDROME

Weakness: Variable
Ocular: Extraocular muscle (EOM) weakness; Ptosis
Bulbar: Dysphagia
Limb: May be focal in legs or arms
Repetitive contraction: Fatigue after transient increase
Electrophysiology
Decrement at 1 to 5 HZ
Increment: Mild (50%) at 10 to 50 Hz
Repetitive compound muscle action potentials (CMAPs)
MEPPs: Low amplitude with Longer time constant of decay
AChR channel properties altered: Reduced Total current; Slow closure
Pathology
Inflammation: CD3+ T-cells > CD20+ B-cells
Higher # of NMJs on single muscle fiber
Normal number of α-bungarotoxin binding sites
Electron microscopy: Simplification of post-synaptic regions without degeneration of junctional folds
Thymus: Hyperplastic
Anti-AChR antibodies
Borderline titers by conventional assay (Mostly fetal AChRs)
Positive in assay of binding to adult AChRs: ? Recognize epitopes on e-subunit
Treatment
Response to anticholinesterase agents: Variable; Poor to Good
Also see: Hereditary slow channel syndromes