But that doesnt mean that MG is simple to treat, he admits. There are many treatments available to people with the disease and finding the right ones for each patient can be a challenge.

MG is an autoimmune disease, meaning that the immune system turns against the bodys own tissues. In the case of MG, the immune system targets the connection between nerve and muscle, or the neuromuscular junction.

The normal sequence of events between nerve impulse and muscle contraction takes about a thousandth of a second. Nerve cells release a chemical called acetylcholine (ACh), which attaches to a docking site on muscle cells, called the ACh receptor. Once its captured ACh, the receptor actually a pore in the muscle cell twists open, causing an inward flux of electrical current that triggers muscle contraction. These events are terminated (at least in part) by acetylcholinesterase, an enzyme that breaks down ACh in the space between the nerve ending and the muscle cell surface.

In most cases of MG, the immune system makes antibodies that recognize the ACh receptor. The antibodies, Y-shaped missiles that normally attack bacteria and viruses, destroy many of the ACh receptors on muscle. Consequently, the muscles response to repeated nerve stimulation declines with time, causing weakness and fatigue.

Of course, none of this was known in the late 19th century, when MG was first described in detail. Understandably, the outlook for patients was grim; in fact, the name of the disease, which literally means "grave muscular weakness," was chosen to emphasize its severe, often fatal course. Even in the early 20th century, many people with MG lost strength rapidly within a year or two of diagnosis, and they ultimately died of respiratory failure.

In the 1930s, the role of ACh at the neuromuscular junction was discovered, and soon, cholinesterase inhibitors drugs that block the breakdown of ACh by acetylcholinesterase became a standard treatment for MG. In the 1960s, researchers discovered the autoimmune nature of MG, and began attacking the disease at its roots using immunosuppressant drugs.

Today, thanks to these treatments and others, its estimated that the mortality rate of MG is less than 5 percent.

Experts say the first step toward getting effective treatment for MG is an accurate diagnosis.

Double vision and droopy eyelids might lead a physician to suspect MG. Weakness of the extraocular muscles, those that control movement of the eyes and eyelids, is conspicuously absent in many neuromuscular diseases, but its a common and early symptom of MG.

For about 15 percent of people with MG, the disease remains exclusively "ocular" for its entire course, but for most people, it eventually becomes "generalized," involving voluntary muscles throughout the body. If left untreated, weakness often spreads from the extraocular muscles to the rest of the face (including the jaw, throat, and tongue), then to the limbs and trunk, and finally to the respiratory muscles.

Weakness that fluctuates during the day and over longer periods, from months to years, is another hallmark of MG. But other diseases can cause similar symptoms, and to the untrained eye, some of these can look a lot like MG.

The most reliable indicator of MG is a blood test that reveals antibodies to the ACh receptor, says Daniel Drachman, director of the MDA clinic at Johns Hopkins University in Baltimore.

But that test isnt foolproof, Drachman points out. "Weve known for a long time that people with mild MG may have no ACh receptor antibodies, and that as many as 15 percent with generalized MG dont have the antibodies," Drachman admits.

A 2001 study showed that many of these seronegative MG patients have antibodies to MuSK, a protein that helps organize ACh receptors on the muscle cell surface. Unfortunately, blood tests for detecting the MuSK antibodies arent yet commercially available.

If the blood test for ACh receptor antibodies is negative, the next step is usually electromyography (EMG), which involves using electrodes to measure a muscles response to nerve impulses. Edrophonium (Tensilon), a fast-acting cholinesterase inhibitor, might be given as a test to temporarily improve neuromuscular transmission.

Finally, "Its key to distinguish MG from congenital myasthenic syndromes," Drachman says. These diseases related to but different from MG are caused by genetic defects in the ACh receptor and other components of the neuromuscular junction, and thus can share symptoms with MG. Some even respond well to cholinesterase inhibitors, but they arent treatable with immunosuppressant drugs.

A family history of myasthenic symptoms, childhood onset and a seronegative blood test for MG generally favor a diagnosis of CMS.

Once a diagnosis of MG is established, both doctor and patient face many decisions regarding treatment. Most of the available medications and procedures have side effects, from mood changes to gastrointestinal problems, and a few have been linked to more serious ailments, including osteoporosis and kidney damage.

The balance between risk and benefit must be weighed separately for each patient, Wolfe says.

In addition, he says, "you have to factor in the patients perspective on their disease on how well theyre functioning now and what things theyd like to be able to do better." For example, someone who has a physically demanding career might prefer an aggressive, risky treatment over a less risky, slower-acting treatment; someone whos retired might prefer the opposite.

Donald Sanders, director of the MDA clinic at Duke University in Durham, N.C., says that, all things considered, cholinesterase inhibitors are usually the first-line treatment for MG. These drugs, which include pyridostigmine (Mestinon) and neostigmine (Prostigmin), can alleviate symptoms within minutes, and have no major side effects, he points out.