There are approximately 60,000 patients with myasthenia gravis in the United States. Although once a severe and often fatal illness, myasthenia gravis can now be managed with several partially effective therapies. Management involves a graded approach, beginning with cholinesterase inhibitors for mild symptoms and advancing to immunomodulating medications for more severe weakness.
Myasthenia gravis treatment with
Very little research is available regarding the alternative treatment of MG.
Creatine, a nutrient involved in increasing muscle mass and strength has been found to be helpful.
Effects of resistance exercise and creatine
supplementation on myasthenia gravis: a case study.
Stout JR. Exercise Science Department, Creighton University, Omaha, NE. Med Sci Sports Exerc. 2001.
The purpose of this case study was to determine the effects of 15 wk of resistance exercise and creatine (Cr) supplementation on body composition, training volume, peak strength, and complete blood chemistry in a patient with myasthenia gravis. The patient was a 26-yr-old man who was taking prednisone and azathioprine for his condition. The patient self-administered 5 g of creatine per day in addition to resistance exercise 3 times per week. Fasting blood samples were obtained and body weight (BW) and fat free mass were measured before and after training and Cr supplementation. In addition, isokinetic (Cybex II) peak strength for leg extension (LE), leg flexion (LF), and volume load (repetition x mass lifted) for the first and last resistance training session were determined. After creatine supplementation and training, the results demonstrated increases in BW (6%), fat free mass (4%), upper body volume load (37%), lower body volume load (15.0%), and peak strength for LE (37%) and LF (12%). Moreover, blood chemistry values remained within normal limits for the duration of the 15-wk study. These data suggest that resistance exercise plus creatine supplementation may promote gains in strength and fat free mass in patients with myasthenia gravis. myasthenia gravis.
Zhongguo Zhong Yao Za Zhi. 2009
Research advances of Huperzia serrata.
Qiancengta, a traditional Chinese medicine produced from the whole plant of the club moss Huperzia serrata, has been used for a long history in China for treatment of a number of ailments, including contusions, strains, swellings, schizophrenia, myasthenia gravis and noworganophosphate poisoning. It has become known worldwide as a medicinal plant since Chinese scientists discovered huperzine A from it in the 1980s, which is reversible, potent and selective acetylcholine esterase (AChE) inhibitors by in vitro and in vivo pharmacological, and produce definite effects in the treatment of Alzheimer's disease. Now, Qiancengta is popular in all over the word for his famous pharmacological actions. For further exploitation this valuable resource under protection of nature environmental, its biological and ecological features, pharmaceutical active ingredients, artificial propagation and in vitro tissue culture, were reviewed, and the sustainable use of Qiancengta natural resource through plant biotechnology was put on the agenda.
Clinical effect of Tripterygiitotorum combined with
prednisone and its effect on serum IL-6 level in treating patients with
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2002.
To explore the clinical effect of Tripterygiitotorum (T II) combined with prednisone in treating patients with myasthenia gravis (MG) and the changes of immune function after treatment. Sixty-eight patients with myasthenia gravis were randomly divided into two groups, the 36 patients in the treated group were treated with T II plus prednisone and the 32 in the control group were treated with prednisone alone. The therapeutic effect, serum interleukin-6 (IL-6) and peripheral B lymphocyte levels were observed. The therapeutic effect in the treated group was significantly higher than that in the control group. There were significant decrease in serum IL-6 and peripheral B lymphocyte in both groups after treatment (P < 0.05), with the decrements more significant in the treated group. The therapy of T II plus prednisone is superior to that of prednisone alone in treating myasthenia gravis, it has a more potent effect of immunosuppression.
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Ocular myasthenia gravis -- What are the optimum nutrition interventions needed? I have a patient who wants to use natural methods.
I have not studied in detail the treatment of ocular myasthenia gravis with natural methods but will keep my eyes open for such research.
Thanks for the great website and all the information. I
am wondering if you are familiar with MG-Tab? Their claim is awesome. I am a
male 59 years old, diagnosed with OMG in October 05, looking for HOPE. I've
ordered, but not yet received their pills.
We had not heard of this product. According to their website, "MG Tab is a completely guaranteed and clinically proven herbal treatment for Myasthenia Gravis. It consists of a formulation consisting of purely natural ingredients based on the Unani (Greek) system of herbal medicine blended together in a specific proportion to fight and treat Myasthenia Gravis. Thousands of patients have been successfully treated with MG Tab over the past few years. MG Tab is a completely outstanding product and there is absolutely no alternative to its unique formula. Had the effectiveness of MG Tab not been proven beyond any doubt, it would not be possible for us to make such a bold claim. The exact proportion of each ingredient has been deliberately kept secret to avoid imitations of our confidential formula. Treatment with MG Tab is very rapid given the nature of the disease and obvious results can be noticed within three months (90 days) of use. A slightly longer period is required for serious myasthenia gravis cases and treatment can last up to four months (120 days). The main ingredients of MG Tab tablets are:
Styrax Benzoin Dryand
Terminalia Chebule (Yellow)
We find these claims difficult to believe. A search of published studies did not reveal any involving Mg-Tab. We have not seen any studies with the individual ingredients and myasthenia gravis. Plus, the company selling this product is breaking the law by making claims that their product can cure or treat an illness. You could take a gamble and buy it, but don't be surprised if you don't get your money back if you return an empty bottle.
My doctor is Wolfgang Grisold in Vienna / Austria.
After he made TENSILON test and ANTIBODY test, which both were positive, he has
diagnosed Ocular Myasthenia Gravis in 2007. He prescribed me than Mestinon 60 mg
3x1, what I have started with. Now I am taking Mestinon 60 mg 4x1, and have
problems and side effects. I know that steroids and immunosuppression are
jouries in unknown, without subsequent possibility to get back on the beginning,
before taking them. From your web site I have learned that you might have some
alternative therapy which could be more effective than present one. So, I am
writing to you with hope that your medication could be right one for my
I have not studied this topic well enough mostly because there is so little research on natural ways to treat this condition.
Can taking CoQ10 (30-50mg daily) reduce the amount of
Mestinon needed for Myasthenia Gravis (ocular)?
I have not seen such studies, so I don't know.
Myasthenia gravis symptoms
This syndrome causes fluctuating skeletal muscle weakness that worsens with use and improves with rest. Myasthenia gravis symptoms involve eye, facial, oral and pharyngeal, axial, and limb muscles in varying combinations and degrees of severity. Initial symptoms include muscle weakness, particularly in the eyes, face and neck. Patients may have difficulty swallowing, chewing or speaking, and may have double vision. Others are fatigue, especially later in the day which can be aggravated by emotional stress, systemic illness such as a viral respiratory infection, menstrual cycle, pregnancy, hypothyroidism or hyperthyroidism, and other factors.
Myasthenia Gravis Cause, diagnosis
The reasons are many, divided initially between those rare congenital myasthenic syndromes, which are genetic, and the bulk of myasthenia gravis, which is acquired and autoimmune. Therapeutic considerations differ for early-onset myasthenia gravis, late-onset, and MG associated with the presence of a thymoma. Most myasthenia gravis patients can be treated effectively, but there is still a need for more specific immunological approaches. It is possible that certain medications, such as statin drugs used to lower cholesterol levels, could aggravate this condition.
J Autoimmun. 2014 Feb 12. Diagnostic and clinical
classification of autoimmune myasthenia gravis. MG is characterized by muscle
weakness and abnormal fatigability. It is an autoimmune disease caused by the
presence of antibodies against components of the muscle membrane localized at
the neuromuscular junction. In most cases, the autoantibodies are against the
acetylcholine receptor (AChR). Recently, other targets have been described such
as the MuSK protein (muscle-specific kinase) or the LRP4 (lipoprotein related
protein 4). Myasthenia gravis can be classified according to the profile of the
autoantibodies, the location of the affected muscles (ocular versus
generalized), the age of onset of symptoms and thymic abnormalities. The disease
generally begins with ocular symptoms (ptosis and/or diplopia) and extends to
other muscles in 80% of cases. Other features that characterize MG include the
following: variability, effort induced worsening, successive periods of
exacerbation during the course of the disease, severity dependent on respiratory
and swallowing impairment (if rapid worsening occurs, a myasthenic crisis is
suspected), and an association with thymoma in 20% of patients and with other
autoimmune diseases such as hyperthyroidism and Hashimoto's disease. The
diagnosis is based on the clinical features, the benefit of the cholinesterase
inhibitors, the detection of specific autoantibodies (anti-AChR, anti-MuSK or
anti-LRP4), and significant decrement evidenced by electrophysiological tests.
In this review, we briefly describe the history and epidemiology of the disease
and the diagnostic and clinical classification.
Myasthenia gravis is arguably the best understood autoimmune disease, and its study has also led to fundamental appreciation of mechanisms of neuromuscular transmission. MG is caused by antibodies against the acetylcholine receptor (AChR), which compromises effective synaptic transmission. It is clear that AChR antibody destruction of the postsynaptic surface is dependent on complement activation. A muscle-specific kinase has been recently found to be an antigenic target in myasthenia gravis patients without antibodies against the AChR. Autoantibody production in myasthenia gravis is a T-cell-dependent process, but how a breakdown in tolerance occurs is not known. In myasthenia gravis there is an interesting differential involvement of muscle groups, in particular, the extraocular muscles.