MDA leads the search for treatments and therapies for myasthenia gravis (MG). The Association also provides comprehensive supports and expert clinical care for those living with MG.
In this section, you’ll find up-to-date information about myasthenia gravis, as well as many helpful resources. This information has been compiled with input from researchers, physicians and people affected by the disease.
As you learn more about MG, always remember that you’re not alone. MDA is here for you and your family, standing ready to provide help and hope. There is a place for you in the MDA MG community.
MDA provides support by:
Once you sign up with your local MDA office , you’ll begin receiving MDA’s quarterly Quest  magazine, where you’ll find news about research and health care, helpful products and devices, social and family issues, and more.
In addition, MDA will keep you informed through e-alerts, educational publications and speakers, seminars, videos and newsletters.
Please know that there’s a role for you in the fight against myasthenia gravis. The MDA community is strong and dedicated, with opportunities for involvement at all levels, such as:
Please know that there’s an important role for every member of the MG community. We urge you to contact your local MDA office  to learn more.
An MG diagnosis doesn’t mean an end to your hopes and dreams. Changes, challenges and adaptations lay ahead, but also opportunity, fulfillment, joy and hope for a future free of MG.
Never forget that MDA is here to help.
|In myasthenia gravis, muscle weakness often first appears in the muscles of the face, neck and jaw. The arm and leg muscles are affected later.|
Myasthenia gravis (MG) is an autoimmune disease — a disease that occurs when the immune system attacks the body’s own tissues. In MG, that attack interrupts the connection between nerve and muscle — the neuromuscular junction.
The disease first appeared in medical reports in 1672, but didn’t earn its name, which literally means “grave muscular weakness,” until the 1880s.
MG causes weakness in muscles that control the eyes, face, neck and limbs. Symptoms include partial paralysis of eye movements, double vision and droopy eyelids, as well as weakness and fatigue in neck and jaws with problems in chewing, swallowing and holding up the head.
Muscle weakness in MG gets worse with exertion and improves with rest. For more, see Signs and Symptoms .
The cause of MG is unclear. Researchers suspect viruses or bacteria might trigger the autoimmune response; the thymus gland also seems sometimes to play a role in the disease.
Although MG is not hereditary, genetic susceptibility appears to play a role in it and other autoimmune diseases. For more, see Causes/Inheritance .
MG affects women more often then men and tends to begin earlier. The average age of onset in women is 28; the average age of onset in men is 42. In about 10 percent of cases, MG begins in childhood (juvenile onset), which tends to progress slowly and has a high incidence of remission.
MG is treatable with drugs that suppress the immune system or boost the signals between nerve and muscle. Surgeries and other procedures are also helpful in many cases. Most people with the disease are able to manage their symptoms and lead active lives, and a few experience remission lasting many years.
MDA-supported scientists in countries around the world are working to reveal numerous facets of MG, from identifying possible causes and triggers  to the disease's molecular underpinnings to specific treatment strategies. For more, see Research .
Myasthenia gravis (MG) weakens and fatigues the body’s voluntary muscles (those we can move at will). It doesn’t damage the musculature of the heart or the gastrointestinal tract.
Early in its course, MG tends to affect the muscles that control movement of the eyes and eyelids, causing ocular weakness. Consequently, a partial paralysis of eye movements (ophthalmoparesis), double vision (diplopia) and droopy eyelids (ptosis) are usually among the first symptoms of MG.
Weakness and fatigue in the neck and jaw also can occur early in MG. This bulbar weakness — named for the nerves that originate from the bulblike part of the brainstem — can make it difficult to talk, chew, swallow and hold up the head.
Bulbar weakness tends to give speech a slurred, nasal quality. It also can lead to frequent choking spells, and make eating unpleasant and tiresome.
In generalized MG, weakness tends to spread sequentially from the face and neck to the upper limbs, the hands and then the lower limbs. It may become difficult to lift the arms over the head, rise from a sitting position, walk long distances, climb stairs or grip heavy objects.
In some cases, weakness may spread to muscles in the chest that control breathing.
Weakness and fatigue in MG tend to fluctuate from day to day, and even during a single day. People with the disease are often strongest in the morning after a full night’s sleep and weakest in the evening.
Over a longer term, the symptoms of MG usually progress, reaching maximum or near-maximum severity within one to three years of onset in most people. In about 15 percent of people, the disease remains ocular, but in most it becomes oculobulbar or generalized. If the disease remains ocular for three years, it usually doesn’t become generalized.
Weakness serious enough to require full-time wheelchair use is not common in MG. Most people, when properly treated, find they can remain physically active.
Remission, a reversal of some or all symptoms, occurs in about 20 percent of people with MG. Usually, the remissions are temporary, with an average duration of five years, but some people experience more than one remission during their lifetime. A few people have experienced apparently permanent remissions, lasting more than 20 years.
Compared to adult-onset MG, juvenile MG tends to progress more slowly and has a higher incidence of remission. Historically, many children given diagnoses of juvenile MG turned out to have a congenital myasthenic syndrome .
Weakness and fatigue are common complaints in the general population, but the degree and pattern of these symptoms — particularly diplopia, ptosis and other signs of weakness in the eye muscles  — should alert a neurologist to the possibility of myasthenia gravis (MG).
A neurologist will ask many questions and conduct a physical exam to determine the extent of weakness. To look for evidence of increased weakness following exertion, a neurologist might ask the patient to look up without blinking for one or two minutes, hold the arms out for as long as possible or climb up steps.
If the physical exam is consistent with MG, the neurologist usually orders a blood test designed to detect antibodies to the ACh receptor. A blood test for MuSK antibodies is also available. Positive test results confirm a diagnosis of MG.
If the blood tests are negative, the next step is usually electrodiagnostic testing, in which electrodes are used to measure the electrical signals in muscle. Surface electrodes (similar to those used in electrocardiograms) deliver small shocks to a nerve in the arm, leg or face, while other surface electrodes record the responses in muscle. In MG, a muscle’s response to repeated nerve stimulation declines rapidly.
In addition to or in place of electrodiagnosis, the neurologist might try giving an intravenous injection of edrophonium (Tensilon), a fast-acting cholinesterase inhibitor . (Cholinesterase inhibitors are used in the treatment of MG.) A temporary increase in strength after this "Tensilon test" is consistent with MG.
If a diagnosis of MG is confirmed, a CT scan, chest X-rays or magnetic resonance imaging (MRI) will be used to examine the thymus and look for evidence of a thymic tumor, which occurs in about 15 percent of people with MG.
|Normally (A), the immune system releases antibodies to attack foreign invaders, such as bacteria. In autoimmune diseases (B), the antibodies mistakenly attack a person’s own tissues. In myasthenia gravis, they attack and damage muscle cells.|
|Myasthenia gravis occurs when the immune system makes antibodies that destroy the ACh receptor (AChR), a docking site for the nerve chemical acetylcholine (ACh). Some treatments block acetylcholinesterase (AChE), an enzyme that breaks down ACh, while others target the immune system.|
The immune system normally defends the body against diseases, but sometimes it can turn against the body, leading to an autoimmune disease. MG is just one of many autoimmune diseases, which include arthritis and type 1 diabetes.
In all of these diseases, an army of immune cells that would normally attack bacteria and disease-causing "germs" mistakenly attacks cells and/or proteins that have essential functions in the body. In most cases of MG, the immune system targets the acetylcholine receptor — a protein on muscle cells that’s required for muscle contraction (see illustration to the right).
At the normal neuromuscular junction, a nerve cell tells a muscle cell to contract by releasing the chemical acetylcholine (ACh). ACh attaches to the ACh receptor — a pore or "channel" in the surface of the muscle cell — twisting it open and allowing an inward flux of electrical current that triggers muscle contraction. These contractions enable someone to move a hand, to dial the telephone, walk through a door or complete any other voluntary movement.
About 85 percent of people with MG have antibodies against the ACh receptor in their blood. The antibodies (Y-shaped missiles that immune cells called B cells use to attack bacteria and viruses) target and destroy many of the ACh receptors on muscle. Consequently, the muscle’s response to repeated nerve signals declines with time, and the muscles become weak and tired.
About 15 percent of people with MG are seronegative for antibodies to the ACh receptor, meaning the antibodies aren’t detectable in their blood (serum). Recently, it’s been discovered that a large fraction of these people have antibodies to muscle-specific kinase (MuSK), a protein that helps organize ACh receptors on the muscle cell surface.
Scientists don’t know what triggers most autoimmune reactions, but they have a few theories. One possibility is that certain viral or bacterial proteins mimic "self-proteins" in the body (such as the ACh receptor), stimulating the immune system to unwittingly attack the self-protein.
There's also evidence that an immune system gland called the thymus plays a role in MG (see illustration below). Located in the chest just below the throat, the thymus is essential to the development of the immune system. From fetal life through childhood, the gland teaches immune cells called T cells to recognize self from non-self.
|The thymus, a small gland in the upper chest, seems to play a role in myasthenia gravis.|
About 15 percent of people with MG have a thymic tumor, called a thymoma, and another 65 percent have overactive thymic cells, a condition called thymic hyperplasia. When the thymus doesn’t work properly, the T cells might lose some of their ability to distinguish self from non-self, making them more likely to attack the body’s own cells.
Although MG and other autoimmune diseases are not hereditary, genetic susceptibility does appear to play a role.
Most studies suggest that if you have a relative with an autoimmune disease, your risk of getting an autoimmune disease is increased — the closer the relative, the higher the risk.
Even for identical twins, however, that risk is relatively small. Most studies suggest that when one twin has an autoimmune disease, the other has less than a 50 percent chance of getting the same disease.
Also, people who already have one autoimmune disease have a greater risk of developing another one. It’s estimated that 5 to 10 percent of people with MG have another autoimmune disease, which appeared before or after the onset of MG. The most common of these are autoimmune thyroid disease, rheumatoid arthritis and systemic lupus erythematosus (a disease that affects multiple organs).
Many drugs and procedures are available for treating MG, each with distinct advantages and disadvantages. Drugs known as cholinesterase inhibitors provide relief from symptoms by blocking the action of acetylcholinesterase and increasing the amount of acetylcholine at the neuromuscular junction. (For a more detailed explanation of how these drugs work, see Causes/Inheritance .)
Immunosuppressant drugs can be used to attack the disease at its source, but they increase susceptibility to infectious diseases and most of them carry other potentially serious side effects.
The benefits and risks of these treatments must be weighed against each other and the needs of the patient. Your doctor or MDA clinic  director can help you determine which treatments are appropriate for you.
These drugs, also known as anticholinesterases, have been used against MG since the early 1990s, and can produce relief from symptoms within minutes. The one most commonly used is pyridostigmine (Mestinon).
Cholinesterase inhibitors boost ACh levels not only at the neuromuscular junction but also in the autonomic nervous system (which controls involuntary bodily functions). Sometimes the drugs can cause diarrhea, abdominal cramps and/or excessive saliva. To minimize these side effects, your physician might lower the dose of cholinesterase inhibitors or prescribe atropine, which blocks the ACh receptors on nerve cells.
In rare cases, cholinesterase inhibitors prove sufficient for managing MG, but most people also require immunosuppression — treatment that restrains the actions of the immune system.
Back to top 
Many prescription drugs can unmask or worsen symptoms of MG. These include:
When taking a new prescription drug for the first time, it’s a good idea to consult your doctor about its possible effects on MG. Also, you might want to keep a MedicAlert bracelet or card handy to inform emergency medical personnel that you have MG and that certain drugs can be harmful to you.
Overexertion, emotional stress, infections (from tooth abscesses to the flu), menstruation and pregnancy  also can lead to increased weakness in MG.
Back to top 
Corticosteroids. These drugs (which include prednisone and prednisolone) reproduce the actions of corticosteroid hormones, which are made by the cortex (outer layer) of the adrenal gland. They have broad anti-immune and anti-inflammatory effects, making them powerful treatments for MG.
They’re not as fast-acting as cholinesterase inhibitors, but they’re faster than some other immunosuppressants, producing improvement within weeks to months. They’re also relatively inexpensive.
A disadvantage of corticosteroids is that they can produce many side effects — some of them potentially serious — including osteoporosis (weakening of bones), mood disturbances, gastrointestinal problems, weight gain, high blood pressure, cataracts and stunted growth (in children). For many people, these side effects can be managed with other therapies; for example, bisphosphonate drugs can be used to prevent osteoporosis.
For others, corticosteroids are used as a first-line defense against MG, then gradually tapered off, and supplemented or replaced with slower-acting immunosuppressants that have fewer side effects. Most of these other drugs were developed to prevent the rejection of transplanted organs, but have since been co-opted for use against MG and other autoimmune diseases.
Azathioprine (Imuran). This was the first non-steroid immunosuppressant to come into widespread use against MG, in the 1970s. It acts more slowly than corticosteroids, producing improvement after three to six months, and usually has few side effects. Occasionally, however, it can produce serious side effects, including inflammation of the pancreas, liver toxicity, bone marrow suppression and possibly an increased risk of cancer.
Mycophenylate mofetil (CellCept). CellCept is a relatively new immunosuppressant, but so far it’s shown promising results against MG in clinical trials. In two small trials completed in 2001, about 65 percent of MG patients experienced gains in strength or a reduced need for prednisone after taking CellCept for several months.
More recent analyses have shown that some people take longer to respond to the drug, but that nearly 75 percent eventually show improvement, with occasional relatively nonserious side effects such as stomach upset, flulike symptoms, rash and tremor.
Cyclosporine (Neoral, Sandimmune). This is a useful, relatively fast-acting treatment for MG, but it may have side effects including increased blood pressure, abnormal kidney function, unwanted body hair and stomach upset.
Cyclophosphamide (Cytoxan, Neosar). This drug is considered effective against MG, but because it has many potentially serious side effects, it’s often reserved for use only when other drugs fail.
Back to top 
Especially in people with bulbar or respiratory symptoms, MG can sometimes worsen to the point of myasthenic crisis, an extreme episode of weakness that culminates in respiratory failure and the need for mechanical ventilation. In some cases, the respiratory muscles themselves give out, and in others, weakness in the throat muscles causes the airway to collapse.
When MG is properly treated, crisis is very rare. And when crisis does occur, it has a good rate of recovery, thanks to the wide range of treatments for MG and the quality of respiratory care at most hospitals.
Sometimes, myasthenic crisis can occur without warning, but it often has an identifiable trigger, such as fever, respiratory infection, traumatic injury, stress, or one of the drug types mentioned above. If you have MG, you should have these conditions monitored by a physician, and if you experience labored breathing or unusual weakness, you should seek immediate medical attention.
Back to top 
In plasmapheresis , also known as plasma exchange, an intravenous line is used to remove antibodies from the blood. IVIg therapy is essentially an injection of nonspecific antibody (immunoglobulin) that might work by dialing down the immune system’s production of its own antibodies, much as warm air tells a thermostat to stop pumping out heat.
These treatments bring about fast, but short-lived relief from MG, and are mostly used until other medications take effect, prior to surgery or for myasthenic crisis. However, some people receive regular plasmapheresis or IVIg as a supplement to immunosuppressant drugs.
Back to top 
In rare cases, pregnancy appears to trigger the onset of MG. In women who already have MG, pregnancy can cause a worsening of symptoms (usually after birth, but sometimes during the first trimester); an improvement (usually during the first trimester); or no change, with about equal likelihood. These trends aren’t consistent from one pregnancy to the next.
Some medications for MG are safe to use during pregnancy and nursing, but some others aren’t recommended. If you’re planning to become pregnant, you should consult your physician, and if you’re a nursing mother, consult your child’s pediatrician.
Between 10 and 20 percent of babies born to mothers with MG develop transient neonatal MG, probably because the antibodies that cause MG can pass through the placenta. Symptoms (such as feeble cry, feeding difficulties or respiratory weakness) often are detected within hours to days after birth, and decreased movement may be detected inside the womb.
As the name implies, transient neonatal MG is only temporary. Most babies require medication and supportive care, but usually recover completely within two months after birth. Permanent weakness or recurrence of MG later in life is extremely rare.
Back to top 
Thymectomy — surgical removal of the thymus gland — is recommended for thymoma and for most cases of generalized MG. It’s believed to be the only therapy capable of producing long-term, drug-free remission from MG, but most data regarding its use have come from case studies rather than clinical trials.
Thymectomy is estimated to produce remission from MG in about 30 percent of people. It’s also known to increase strength or reduce the need for medication in an additional 50 percent. These improvements may take several months to several years after surgery to occur.
Thymectomy usually has the most favorable outcomes in people who are under age 60 and early in the course of the disease. Because the thymus is required for immune system development, most doctors prefer not to perform the surgery on prepubescent children.
Back to top 
For more about myasthenia gravis management, see:
MDA’s commitment to research on myasthenia gravis began many years ago when little was known about the cause of MG and its mortality rate was high.
In the early 1970s, MDA-funded researchers helped establish the autoimmune nature of MG. They showed that people with the disease have a reduced number of ACh receptors, and that antibodies to the receptors can induce MG in laboratory animals.
These discoveries led swiftly to the lifesaving use of immunosuppressant drugs to treat the disease.
MDA-funded researchers also developed plasmapheresis  as a treatment for MG. Today, they are refining plasmapheresis so that it only sifts out the unwanted antibodies, not the ones that are doing their job properly.
Today, several MDA-supported research teams are working to understand the specifics of the autoimmune problems in MG and to refine their detection and treatment. A particular area of focus is "rebalancing" the immune system, rather than the earlier approach of suppressing it. One way to rebalance the overactive immune system is by enhancing the activities or numbers of so-called regulatory T cells, which dampen an immune response that has gotten out of hand.
Another important area of current research is understanding the physiology of the neuromuscular junction, with the goal of improving its function despite an immune system attack on it.
Read New Directions: Can an immune response be rerouted to treat disease?  and MG: Can the Immune Response Be Tamed?  to learn more.
A clinical trial is a test in humans of an experimental medication or therapy. Clinical trials are experiments, not treatments, and participation requires careful consideration.
Although it's possible to benefit from participating in a clinical trial, it's also possible that no benefit — or even harm — may occur. Keep your MDA clinic  doctor informed about any clinical trial participation. (Note that MDA has no ability to influence who is chosen to participate in a clinical trial.)
For more about clinical trials in general, see Learn About Clinical Studies , and to learn more about trial participation in neuromuscular disease, read the Quest magazine article Being a Co-Adventurer .
For a more refined list of MG clinical trials, visit ClinicalTrials.gov , a registry of federally and privately supported clinical trials in the United States and around the world. Select "Search for Clinical Trials," and follow the instructions to narrow down your search results.
In 1997, I started to feel weak and tired all the time, especially in my neck. Basic functions that I'd always taken for granted — like chewing, swallowing and talking — suddenly became difficult. One of my eyes began to droop and my arms felt weak.
I hoped these were signs of some temporary illness, but my symptoms continued and, finally, physicians at an MDA clinic  near my home discovered I had myasthenia gravis.
About three years after this diagnosis, I became quite ill and required a variety of medications, therapies and treatments prescribed by my doctors. I worried about how having this disease would affect my future, my family and my career as a pediatric psychotherapist, which requires a lot of talking with clients and health care professionals.
The good news is, I've essentially recovered; I’ve been able to resume a full schedule at work, with a few accommodations to help me conserve my energy, and to continue to do my home gardening, which I love. Now, I don't worry so much about MG.
If you or someone you love has just received a diagnosis of MG, you'll learn, as I did, that a variety of treatments can be used to control it. By learning more about MG and by partnering with your physician, you'll discover that you can become an active participant in your treatment plan, adjust to your diagnosis and take control in maintaining the quality of your life.
These MDA myasthenia gravis information pages will provide you with essential information about the symptoms of MG and the best treatments for it, which are different for each person.
You'll learn that MG causes progressive weakness and fatigue in the body’s voluntary muscles, without affecting the musculature of the heart. Although it can weaken the muscles that control breathing, MG usually doesn't shorten life expectancy. You'll find details about these treatments — from drugs to surgery and other procedures — that will help you discuss your options with a physician.
The Muscular Dystrophy Association can help guide you through this process in many ways. The doctors at my MDA clinic have established an appropriate course of treatment. I visit the clinic regularly, and they continue to adjust the treatment to any changes in my needs. The local MDA staff were there for me on the day I was diagnosed and have been available for support ever since.
Since my diagnosis many years ago, I've continued to work, and my husband and I have raised two children who are now adults. I lead a very active life and in addition to my gardening, I enjoy community service, sailing, travelling and the arts. At times, I've had to make adjustments. When I've had episodes of extreme weakness, my family has been there to help me.
Changes at work can be challenging, but remember: If you have lasting or recurring disability from MG or any other disease, the law entitles you to reasonable workplace accommodations and equal employment opportunities.
And remember that MDA is here to help. If you have unanswered questions, contact a member of your local MDA staff. With the help of the MDA staff and others who understand your illness, this is a journey that you don't have to take alone.