Talk:Myasthenia gravis

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Myasthenia gravis was a good article nominee, but did not meet the good article criteria at the time. There are suggestions below for improving the article. Once these are addressed, the article can be renominated. Editors may also seek a reassessment of the decision if they believe there was a mistake.

Reviewed version: April 24, 2007

Contents

[edit] Marijuana

Has there been any research done about this disease and it's relationship to marijuana abuse?

Why are you asking? Have you tried google or the reference desk? JFW | T@lk 16:08, 9 December 2007 (UTC)

[edit] Help

Answer:

Dear Freazer,

I consulted several neurologists, a neurophysiologist, a research group looking for new medicines for MG, a patients association and the original author when improving the article. I suggest we collaborate to make a good article, in stead of reverting to older versions. For most changes i made i had good reasons, so perhaps you can discuss any changes you don't agree with, in stead of undoing all the effort that was put in it. It is very unfortunate that the article became victim to vandalism since february 1st so i suggest we both try to keep it vandalism-free. Perhaps we the wiki group can make editing members-only. Anyway, my changes were not vandalism.

The reason i added section you mentioned: As i see it, this article is intended to give information to people who want information about myasthenia gravis. That will mostly be patients, their friends and relatives and doctors, nurses and researchers. I also added a lot of information useful for doctors and researchers. But to patients thís is very useful info, and imo adding info like this makes the wiki better than any other encyclopedia. Because it actually answers one's questions. Nevertheless i left the section out, since it especially seemed to bother you. Hope to hear from you soon; you can mail me at arendhamming(at)gmail(dt)com.

Pizzaman79 11:31, 9 March 2007 (UTC)

[edit] I doubt this

The article says: Applying ice to the weak muscle groups may characteristically improve the weakness. Is this true?

Yes, this factlet is specifically supported by the Scherer reference. JFW | T@lk 13:26, 22 December 2005 (UTC)
Yes, cooling increases the sensitivity of the postjunctional membrane to acetylcholine and decreases cholinesterase activity. (Nerve conduction speed and acetylcholine release are decreased by cooling and these adversely affects neuromuscular transmission. This, however, is partially counteracted by decreased muscle-ChE activity and increased sensitivity of the postjunctional membrane to ACh caused by cooling. In MG patients these last two effects have a much greater effect than in healthy individuals and neuromuscular transmission actually improves. See also PMID 690633) --WS 14:04, 22 December 2005 (UTC)

[edit] Myasthenia is derived from Greek; Gravis is from Latin

From the top of the page:

Myasthenia gravis (MG, Latin: "grave muscle weakness")

See

http://www.lef.org/protocols/prtcl-080.shtml

Myasthenia: from the Greek words, myelos, meaning muscle, and astheneia, meaning weakness Gravis: from the Latin word, gravidus, meaning heavy (serious) —Preceding unsigned comment added by 62.25.109.194 (talk • contribs)

Thank you for your suggestion regarding [[: regarding [[:{{{1}}}]]]]! When you feel an article needs improvement, please feel free to make whatever changes you feel are needed. Wikipedia is a wiki, so anyone can edit almost any article by simply following the Edit this page link at the top. You don't even need to log in! (Although there are some reasons why you might like to…) The Wikipedia community encourages you to be bold. Don't worry too much about making honest mistakes—they're likely to be found and corrected quickly. If you're not sure how editing works, check out how to edit a page, or use the sandbox to try out your editing skills. New contributors are always welcome. --WS 13:09, 11 January 2006 (UTC)

[edit] Re-write of Prognosis section

First, I wish to declare my bias, so you can call me on it if I let it affect my contributions. I have a friend who's been diagnosed with MG and her friends are visiting wikipedia for a quick summary. Unfortunately, the "Prognosis" section gives the impression MG is completely treatable, which is not true. When I went digging I found the origins of the pronosis section:

With treatment, most patients have a near-normal quality of life and no significant problems. Some cases of myasthenia gravis may go into remission temporarily and muscle weakness may disappear completely so that medication can be discontinued. Stable, long-lasting complete remissions are the goal of thymectomy, although this cannot always be achieved. (Wikipedia, current version)

It appears to be based on a factsheet from the US government, aimed at patients:

With treatment, the outlook for most patients with myasthenia gravis is bright: they will have significant improvement of their muscle weakness and they can expect to lead normal or nearly normal lives. Some cases of myasthenia gravis may go into remission temporarily and muscle weakness may disappear completely so that medications can be discontinued. Stable, long-lasting complete remissions are the goal of thymectomy. In a few cases, the severe weakness of myasthenia gravis may cause a crisis (respiratory failure), which requires immediate emergency medical care. (see above). (Fact Sheet).

The fact sheet is careful not to alarm people, but the wikipedia entry omits all negative information. Overall, the wikipedia entry gives a very rosy picture. Now I'm going to try and re-write that section based on other sources.

geoff_o 21:50, 26 October 2006 (UTC)

I think from a doctor's perspective there are many worse, less treatable diseases. Especially from a neurologist's perspective. I agree it should not sound too optimistic. On the other hand i see a lot of patients that googeled their disease and then come to the doctor with their heads full of worst case scenario's. Sometimes to the point where these thoughts bother the patient even more than the disease itself! So it's always difficult to strike a balance. If the update i did on the english version is read and corrected, i'll translate it to Dutch. Then i'll try to get some dutch patients to look at it, i'm already in contact with the dutch foundation for muscle diseases. If i get the opportunity i'll specifically ask them about their experiences. Pizzaman79 13:33, 13 December 2006 (UTC)

[edit] Details

I just did a few months of research with the dutch MG expert, Dr De Baets (MD). This is a great article, but i think it misses some details here and there. I could ask De Baets to help me look into it, but i'm only going to ask him to spend some of his valuable time if the guys from wikipedia are going to lock it afterward. Some examples...

- The autoimmune process is NOT fully clarified imho. First of al some of the patients don't carry AchR or MuSK antibodies. Since they do respond to immunosuppresive therapy they probably have some other, yet unknown, auto-immune process. Also, MG seems different from other autoimmune diseases. Some genetical variations (SNP's) seem to have effects opposite to other auto immune diseases, sometimes ascribed to T-cell maturation in the thymus.

- The stuff about ice is a very neat trivia. But a reader will think this is the common way doctors examine patients and it's not. So that should be clarified. What i miss is an explenation about which tests doctorsactually do. For example, just asking a patient to keep his arms stretched out (Barré style) will clearly show fatiguability of a muscle with otherwise good strength (usually 5/5). I have an book about MG by Oosterhuis, i should look up what he sais in his chapter about the physical exam.

- The part on the blood test could state more clearly that the diagnostical use of the test is limited. The ultimate test is a patient's response to immunosuppressive therapy, in my experience. Also, wasn't the antibody titer useful for followup? (i'd have to look that up)

- Pathophysiology: again too optimistic to my taste. Even when testing for MuSK there are still sero-negative patients and i believe the MuSK test is not something many hospitals offer. Without that you'll have quite a lot of seronegative patients. (i'm not even sure if the AchR test is that common)

- Epidemiology: do we have figures about congenital MG? Also there are two epidemiologic peaks: females in their 30's and males in their 50's and 60's. This suggests perhaps hormonal influence or two distinct entities and should therefor be mentioned.

- I think if you mention thymectomy and chest (thymus) CT's for thymoma imaging, you should also explain the correlation a little more thorough than "There are various theories that explain why thymoma may predispose to MG"

These are just some things that cought my eye in a first quick read. Since i'm suggesting a lot more than a few minor changes i suggest the original author can contact me so we can perhaps collaborate on a rewerite.

Edit: i contacted the original author and another person doing research on the topic. It may take some time, but i'll do a rewrite.

Edit2: I changed the article now. It didn't need as much changing as i first expected. One point of discussion remains: prevalence. I have a neurology book stating it is 40/million, whereas myasthenia.org says 20/100.000 is an underestimation! Who can find an authorative reference?

Pizzaman79 03:31, 11 December 2006 (UTC)

I think improvements can be made to the Neurophysiological changes associated with the disease. SteveD 16:08 13 April 2008.

As an MG patient, I would think that myasthenia.org would have more recent info, however, as it is with everything realted to MG, I think a 100% accurate info is not available. Bengisuk 10:53, 9 February 2007 (UTC)

Agreed.

[edit] Good article nomination

Here are my suggestions:

  • "At about 14 cases per 100,000 (in the U.S.), it is one of the lesser known autoimmune disorders." (reference?)
  • According to Wikipedia:Manual of Style (medicine-related articles), classification should be placed before Signs and symptoms.
  • "Often the physical examination is within normal limits." (a reference about an overview of the signs would be welcome)
  • "Often symptoms come and go. The diagnosis of myasthenia gravis is often initially missed." (I don't think it's a proper sentence, you can't write that symptoms come and go)
  • Reference for the classification?
  • Please follow the manual of style regarding the order of sections
  • and most of the diagnostic tests are unreferenced sections
  • external links in the sections should be converted into references (see Epidemiology)
  • I don't think we should include specific doses.

Thank you in advance! NCurse work 16:58, 13 April 2007 (UTC)

No response to the hold, so I'm failing the GA on this. Please renominate if the concerns are addressed. Thanks Mike Christie (talk) 22:24, 24 April 2007 (UTC)

[edit] Thymectomy survey

I think this article would benefit from a mention of the large-scale survey into the effectiveness (or otherwise) of thymectomy, led by John Newsom-Davis until his recent sudden death. I was tempted to add something myself, but I think it would be better done by an expert in the field.
--NSH001 14:20, 10 October 2007 (UTC)

If the results were published, please provide a reference. If the results have not been published, I'm afraid WP:NOR applies. JFW | T@lk 16:08, 9 December 2007 (UTC)
(interrupting my wikibreak for a few moments - I won't be able to respond again for a while) There are plenty of refs in the JN-D article, and I'm sure google will provide a few more. I expect it'll be a while before full results are published, but some mention of the scope of, and reasons for, the survey would, I think, be appropriate.
--NSH001 (talk) 16:54, 9 December 2007 (UTC)

[edit] References

The following references were listed at the bottom of the article:

  • Baets, MH de, Oosterhuis HJGH. Myasthenia gravis. Boca Raton: DRD Press, 1993
  • Rowland LP, ed: Merritt's textbook of Neurology. 10th Ed. Philadelphia, Lippincott, Williams & Wilkins, 1995
  • Cavel-Greant, D, Nicolle, MW ed; You, Me and Myasthenia Gravis Third ed. Ku:Reh Press, 2006

Generally, we are now avoiding article references. I have listed them here for other users to peruse while I try to update the article using recent journal reviews. JFW | T@lk 16:08, 9 December 2007 (UTC)

Apart from Conti-Fine et al, I have identified the following free reviews:
Not free: the entire first issue of Semin Neurol 2004: Pubmed search
PMID 11494281 - electrodiagnostic evaluation.
PMID 11445126 - Lancet seminar (2001)
JFW | T@lk 16:49, 9 December 2007 (UTC)

[edit] Pathophysiology section -revision of statements about normal physiology needed

The fourth paragraph under "Pathophysiology" is factually incorrect:

"In normal muscle contraction, cumulative activation of the ACh receptor leads to influx of sodium and calcium. Only when the levels of these electrolytes inside the muscle cell is high enough will it contract. "

Not so. Each activation of the ACh receptor (at the neuromuscular junction by means of the ACh released by each arriving motor action potential) opens a sodium-potassium permeable 'non specific' ion channel. This leads to a depolarisation of the muscle fibre membrane under the motor end-plate. Calcium entry is not favoured by ACh, but critically the 'levels of these electrolytes' (be they sodium and potassium) are not appreciably altered. It is the (small) flux of the ions across the membranes that carries and electric current sufficient to depolarise that local region of membrane. The 'levels' (concentrations) of sodium and potassium are not altered appreciably as a result of one, or indeed many action potentials. The depolarisation triggers an action potential in the muscle fibre which, in turn, triggers the release of calcium from internal stores in the muscle fibre (the sarcoplasmic reticulum). The rise in calcium concentration is what favours contraction.

So the problem of the antagonism of the ACh receptor by antibodies is that the incoming action potential fails to depolarise the motor end plate and thus fails to trigger a new action potential in the muscle fibre. This means there is no response by the muscle to the nerve's activity and hence paralysis. Repeated action potentials may allow sufficient receptors to be activated sufficiently for a response (though it is thereby weakened). This outcome is favoured by the use of anticholinesterase agents which inhibit the breakdown of ACh. The offending antibodies may be competitively antagonised by ACh if it is at a high enough local concentration for long enough. DoctorCaffeine (talk) 13:46, 27 May 2008 (UTC)