Does anyone else do better in the heat?
 

I know most MGers have a lot of trouble in the heat, but I don't. In fact, this is the second spring in a row that I've felt much better when things warmed up, and even really hot days don't bother me (I live in southern New England, and we don't have an air conditioner). Last summer I was even able to go to the ocean and bake in the sun.

My neurologist suggested that my heat tolerance, my seronegativity, and my lack of response to Mestinon might indicate that I have antibodies against a different part of the neuromuscular junction, but that's just speculation. My eye symptoms are also mild-to-none. I've never had ptosis, and only a couple of episodes of double vision (lasting hours) since I first came down with symptoms in October of 2009. I tested negative for MuSK and LEMS, too.

I've been having a "good spell" for several weeks now. Don't know how long it will last--but I'm enjoying it while I can. I don't think I'd say I'm in remission, because I still have symptoms. But I'm able to do things I couldn't a month ago.

Abby

I suspect New England heat is not the same as unrelenting TX heat! Come on down about August and give it a try! Lol.

I actually do quite well until the temps get into the 90s, and even then I don't get really weak, just hot. Over 100 I do have to be careful. My daughter swims on a team so I have tested this out over many summers.

If I can get a chance to cool off periodically I do OK. If not, I do feel the effects after a few hours/days. I've also noticed a big difference in just relaxing and enjoying the sun and say trying to do heavy yardwork in the heat!

Enjoy the good times!

Abby, I am just the opposite of you. I have a lot of eye symptoms daily, constant double vision but my new prism in my eye glasses help a lot. I start feeling bad effects of the heat at 70 degrees, by the time it gets to 90, I can barely walk the 20 yards to the mailbox. I have already had the air conditioning on for weeks. Mestinon gives me good temporary relief. I am seronegative but they have not tested me in a while and my MG has had a steady downward trend.

I think your doctor is right about it being a different antibody. While I was home on disability, I did a lot if research on MG antobodies and found there are a lot more antibodies identified by clinical research with different clinical presentations, But there are no commercially available test of them. if you want i can private message you what I found and the links.

kathie

Hello Abby :) It's always good for us to hear that someone is doing well; it's inspiring, if it's one symptom or ten. Your post shows us how different we can be. I call it, "MG, with a twist." I'm outside the norm on a symptom. More often than not, I improve as the day goes on. Though quite tired around 3:00 to about 6:00pm, I have a general burst of energy in the evening.

Live in Fl-good so far
 

I am just newly diagnosed so I don't have a lot of experience yet. It has gotten to 90 and I am still doing Ok. I don't do yardwork or exercise in the heat. I started with ocular symptoms that progressed to slurred speech, breathing problems and neck weakness. I am seronegative and have not yet been tested for MuSK or LEMS.

Cait-I would love to get those links too, if you don't mind.
Sandy:Grin-Nod:

Fortunatos, I also have that pattern of feeling strong, then tired around 3-6 and then more energy again. I always assumed it was because my kiddo comes home and I have to cook dinner, feed pets, and do other stuff I don't necessarily WANT to do all the time, and once it's done....I'm FREEEEE!!!! :p

:D:D:D I can relate!

....It has gotten to 90... :eek:

....I don't do yardwork or exercise in the heat...

Sandy...What's heat? :D

Sandy, I have been updating a document with all MG antibody info and good MG articles I find. I will try to upload it. I hope it works.

kathie

Kathie I would love to read about the different antibodies. I am positive for 4 so would love to know more.
Mike

I tried to upload the file, but even with breaking it up, it is too big to load. I will try to cut and paste it.

kathie

format:
type receptor abbrev reference link comment
muscle Acethylcholine blocking mACH MG http://www.myasthenia.org/HealthProf...rviewofMG.aspx may impair binding of acetylcholine to the receptor, leading to poor muscle contraction

muscle Acethylcholine binding mACH MG http://cdn.intechweb.org/pdfs/20680.pdf can activate complement mediated membrane damage and lead to loss of AChR.

muscle Acethylcholine modulating mACH MG http://www.hindawi.com/journals/ad/2011/740583/ causes receptor endocytosis (accelerated degredation) resulting in loss of AChR expression, which correlates with clinical severity of disease

neuronal Acethylcholine nACH AAG/ POTS/ AGID http://www.ncbi.nlm.nih.gov/pubmed/10514242 , http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153777/, http://www.neurology.org/content/50/6/1806.short , http://lib.bioinfo.pl/pmid:14732619 , http://www.mayomedicallaboratories.c...nit_code=89886 Autoimmune autonomic ganglionopathy, Autoimmune gastrointestinal dysmotility (AGID)

Muscle specific kinease Musk MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1739764/ , http://neuromuscular.wustl.edu/mtime/mgthy.html predominantly female with more prominent facial and bulbar involvement and more frequent crises. Disease onset tended to be earlier. lack of improvement with, anticholinesterase agents. Somewhat better response was observed with steroids and plasma exchange

titin striated muscle antibody SM Ab MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139883/ Anti-titin antibodies are a sensitive marker of thymoma associated with MG in patients 60 years and younger, seen in other immune disorders. Seen in rippling muscle syndrome which may proceed a MG diagnosis, Respiratory difficulties at MG onset

actnin striated muscle antibody MG http://emedicine.medscape.com/article/1171206-workup also seen in celiac disease

ryanodine striated muscle antibody RyR MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139883/ more common in MG with thymoma, increases the risk for severe MG, highest rate of bulbar, respiratory and neck involvement at MG onset, distinctive non-limb MG symptom profile

Kv1.4 /KCNA4 Voltage-gated K channel VGKC MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139883/ Issacs syndrome, severe MG, thymoma, and concomitant myocarditis and/or myositis

voltage-gated calcium channel VGCC LEMS http://www.privatemdlabs.com/lp/VGCCA_Test.php Lambert-Eaton myasthenic syndrome

low-density lipoprotein receptor-related protein 4 LRP4 MG http://www.ncbi.nlm.nih.gov/pubmed/21814823 , http://www.ncbi.nlm.nih.gov/pubmed/22941261 50% of seronegatice MG have LRP4 antibody

rapsyn MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851878/ , http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2442426/ congenital myasthenic syndrome

collapsin response mediator protein 5 CRMP5 http://www.ncbi.nlm.nih.gov/pubmed/19151024 , http://www.ncbi.nlm.nih.gov/pubmed/18931014 more than twice as frequent, and the antibody levels are higher in patients with thymoma and MG

Transient receptor potential canonical-3 TRPC3 http://www.sciencedirect.com/science...65572808001835 detected in thymoma-associated MG patients

GLUTAMIC ACID DECARBOXYLASE GAD65 http://www.mayomedicallaboratories.c...Overview/81596 , http://www.mayomedicallaboratories.c...rpretive/81596 autoimmune diabetes, stiff‐person syndrome and also in other neurological syndromes, including cerebellar ataxia and epilepsy

Antineuronal nuclear autoantibody-type 1 (ANNA-1) ANNA-1 http://neurology.org/content/59/6/929.abstract Autoimmune gastrointestinal dysmotility (AGID), Seropositive patients usually present with subacute neurological symptoms and signs such as encephalopathy; cerebellar ataxia; myelopathy; radiculopathy; plexopathy; or sensory, sensorimotor, or autoimmune neuropathy, with or without a neuromuscular transmission disorder: Lambert-Eaton syndrome, myasthenia gravis, or neuromuscular hyper-excitability

Wow, thanks, Kathie. I wish we knew more about the different effects of the various antibodies (for example, MuSK tends to have bulbar symptoms and doesn't respond to Mestinon--how about the others?).

This post should be encouraging to seronegative patients who are trying to get a diagnosis. There are a lot of other possibilities besides AChR.

Abby

Heat for me is anything over 80:rolleyes:

I find the best articles under the clinical research:

Annals of the New York Academy of Sciences
© The New York Academy of Sciences, June 2008,
Volume 1132 Myasthenia Gravis and Related Disorders 11th International Conference
Pages 84-92 ,Myasthenia Gravis Seronegative for Acetylcholine Receptor Antibodies

There was a great article where they tested sseronegative ACHR and MUSK MGers by adding Rapsyn ( the thing that makes ACHR receptors cluster) and 60% of the seronegative showed low affinity binding for ACHR antibodies. That means seronegative fit the clinical profile for ACHR Mgers. The test is faulty or not sensitive enough and does not taken into account the heavy clustering of ACHR receptors in the body.

Rapsyn is under investigation as a future treatment for MG. If the ACHR receptors cluster more it is easier to get a muscle action potential and our muscles will work better. At least that is the theory.

I also found another interesting article, I can't find the link now. But it did not consider ACHR antibody a definitive test for MG. It considered, SFEMG, tensilon etc, the definitive test. It said that the antibody tests should be used to profile and subtype the MG to anticipate clinical presentation and treatment response. I think this is a great approach. I wish more neuros used it.

Hope this helps,
kathie

Here is another good article that talks about pain and MG. https://research.wsulibs.wsu.edu/xml...pdf?sequence=1. I know all the common sites say there is not pain with MG, but I have a lot of muscle pain with MG.

There is also another very important point buried around pages 15-16. MG affects skeletal ACHR. But there is also ganglionic and neuronal ACHR which controls the autonomic nervous system like digestion, temperature regulation, hearing etc. In the article it says that after 5 or more years of skeletal antibody production there is some cross-reactivity with ganglionic ACHR. I think this explains my GI symptoms, constant tinitis, dizziness, profuse sweating etc, I think they refer to this as AGID and AAG on my earlier post.

Sorry for the over-analysis, but I am analyst by profession. I need to dig to know the "why".

kathie

I can't handle the heat lol but I'm handling the spring ok. Once it gets to 85/90 degrees, and that lovely humidity kicks in, I'm done, and ready for the AC. My problem maybe more humidity than just being warm, but I do "wilt" a bit in warm weather.