MG results from abnormal immune system activity. Individuals with other auto-immune diseases or an abnormal thymus gland are more likely to have MG. Physicians suspect there may be a combination of factors that trigger the onset of MG symptoms in a susceptible individual, such as an infection or other illness.
Generally, MG is not considered an inherited disease. It is possible for a mother to pass a temporary form of MG to her newborn child. Rarely, the disease does occur in multiple family members.
The gland is somewhat large in infants, grows gradually until puberty, and then gets smaller and is replaced by fatty tissue as a person ages. In some adults with myasthenia gravis, the thymus gland is abnormal and remains large. The relationship between the thymus gland and myasthenia gravis is not yet fully understood. Scientists believe the thymus gland may give incorrect instructions to developing immune cells, resulting in the production of acetylcholine receptor antibodies.
Generally thymomas are benign, but in rare cases they can become malignant. When a thymoma is discovered, surgery to remove it should be performed. MG can be treated with drugs, surgery and other therapies—alone or in combination. Treatment decisions take into account the severity of your disease, which muscles are affected, your age, and other associated medical problems. Click here for details. Many people with MG can live fairly normal lives. The first one to three years — when various symptoms appear — often are the most difficult.
It can take time to work through various treatments to find what works best for you. Symptoms come and go, and periods of remission — when you are symptom-free — are possible. These factors can make your MG symptoms temporarily worse: stress, lack of sleep, illness, overexertion, pain, extreme hot or cold including outdoor temperatures, hot showers or baths, saunas, hot tubs, hot foods or beverages , and some chemicals for instance, in insecticides and lawn treatments.
You should avoid drugs known to make MG symptoms worse, including certain antibiotics, beta blockers, calcium channel blockers, muscle relaxants and magnesium. Be sure to check with your primary MG doctor before taking any new medication, even over-the-counter drugs.
If you live in another state, see if your state has its own MG chapter. They may have a list of neurologists who treat MG. Thymus gland Open pop-up dialog box Close. Thymus gland The thymus gland, a part of your immune system situated in the upper chest beneath the breastbone, may trigger or maintain the production of antibodies that result in the muscle weakness.
Share on: Facebook Twitter. Show references AskMayoExpert. Myasthenia gravis. Rochester, Minn. Clinical overview of MG. Myasthenia Gravis Foundation of America. Accessed April 1, Jameson JL, et al. Myasthenia gravis and other diseases of the neuromuscular junction. In: Harrison's Principles of Internal Medicine.
New York, N. Myasthenia gravis fact sheet. National Institute of Neurological Disorders and Stroke. Simon RP, et al. Motor disorders. In: Clinical Neurology. Jordan A, et al. Recent advances in understanding and managing myasthenia gravis. Bird SJ.
Overview of the treatment of myasthenia gravis. Thymectomy for myasthenia gravis. Accessed April 4, Myasthenia gravis: A guide for patients. Brown AY. Recent studies have shown an increased prevalence of the disease among middle-aged and older patients.
Certainly, most patients with MG receive better treatment today and have a longer life span than ever before. However, the data suggesting a higher prevalence of MG cannot be explained by an accumulation of patients with early onset of the disease who live longer, although in the s the life expectancy of patients with early-onset MG who have undergone a thymectomy does not differ from that of the normal population.
There are also a substantial number of patients who develop the disease much later in life. Three recent studies, from western Denmark, 5 central and western Virginia in the United States, 6 , 7 and Croydon, Great Britain, 8 have demonstrated an increased incidence of MG in the elderly population. Myasthenia gravis has traditionally been regarded as a disorder of young women and older men.
The incidence of MG is still higher among younger women than it is among young men, but recent studies have demonstrated that both sexes now show a bimodal curve for age at onset of MG. The age structure of the population of western societies is changing. Thirty-two percent of the population in the countries of the European Union are older than 50 years. Neurologists will therefore see more patients with late-onset MG than ever before. When does late-onset MG start? Compston et al, 18 in their study, suggested 40 years of age as an arbitrary division.
Somnier et al 14 have pointed out that incidence data are more in favor of separating early- and late-onset MG at the age of 50 years. Late-onset MG is defined herein as the onset of the disease after the age of 50 years in a patient with no clinical or paraclinical evidence of a thymoma but, quite often, with immunological findings similar to those found in patients with thymoma. Is late-onset MG different from early-onset MG?
Yes, in many respects. Thymoma is much more common among middle-aged and older patients. But, even late-onset, nonthymoma MG has characteristics that differentiate it from early-onset disease. Patients with early-onset MG are often DR3 positive and show a high frequency of clinical and serological autoimmune overlap.
Patients with thymoma-associated MG are never, or almost never, DR3 positive, and this haplotype is also uncommon in late-onset MG. The neuromuscular symptoms seen in patients with late-onset MG do not differ from those observed in patients with early-onset MG, although the disease is more likely to be more severe in patients in whom MG develops after the age of 50 years.
The difference in prognosis is probably not related to the size of the tumor, since patients with small thymomas may also have a more serious prognosis. Somnier 21 therefore postulated that the severity of the disease is related to immunological factors associated with the thymoma.
In his study, removal of a thymoma in MG resulted in an exacerbation of the clinical severity of the disease and an increase in acetylcholine receptor antibody titers.
The majority of patients with MG, whether it be of early or late onset, have circulating antibodies to the acetylcholine receptor, but the concentration is often lower in those with late-onset disease.
Patients with late-onset MG with thymus involution who have striated muscle antibodies are immunologically identical to patients with MG with thymoma. While not related to titer, there is a qualitative association of severity to titin antibodies. Somnier and Trojaburg 28 reported that myopathy is more common in patients with late-onset MG than in those with early-onset MG. They also found that the occurrence of myopathy was associated with the presence of anti—striated muscle titin antibodies.
Based on their observations, they suggested that the increased weakness seen in some older patients is caused by an immunologically mediated myopathy and that this could to some extent account for the poorer prognosis in patients with late-onset MG.
Treatment of late-onset MG can be difficult. The effect of acetylcholinesterase inhibitors is often temporary. Plasma exchange has more complications in the elderly.
Keynes, 29 one of the pioneers of surgical treatment of MG, observed that the results of thymectomy were much poorer in the older age group. He also pointed out, and others have confirmed, that patients with thymoma have a worse prognosis.
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