MDA leads the search for treatments and therapies for Lambert-Eaton myasthenic syndrome (LEMS). The Association also provides comprehensive supports and expert clinical care for those living with LEMS.
In this section, you’ll find up-to-date information about Lamber-Eaton myasthenic syndrome, 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 LEMS, 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 LEMS 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 Lamber-Eaton myasthenic syndrome. 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 LEMS community. We urge you to contact your local MDA office  to learn more.
A LEMS 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 Lamber-Eaton myasthenic syndrome.
Never forget that MDA is here to help.
|LEMS symptoms usually begin with leg weakness, often followed by weakness in the muscles of the eyes, face and throat. Sometimes the weakness temporarily improves after exertion.|
Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease — a disease in which the immune system attacks the body's own tissues. The attack occurs at the connection between nerve and muscle (the neuromuscular junction) and interferes with the ability of nerve cells to send signals to muscle cells.
The disease is named for Edward Lambert and Lee Eaton, neurologists at the Mayo Clinic in Rochester, Minn., who first described myasthenic syndrome in the 1950s and '60s.
Initially, LEMS can cause leg weakness and difficulty walking. Like myasthenia gravis (MG) , it also can result in weakness of the eye muscles and those involved in talking, swallowing and chewing.
The main clinical difference between MG and LEMS is that in MG, the person gets weaker with exertion, and in LEMS, the person gets stronger, at least temporarily. For more, see Signs and Symptoms .
In about 60 percent of cases, LEMS is associated with an underlying disease, particularly small-cell lung cancer. It is thought that the body's attempt to fight the cancer inadvertently causes it to attack nerve-fiber endings.
In the other 40 percent of cases, the cause is unknown. For more, see Causes/Inheritance .
LEMS usually appears in middle age, but it also can have its onset in childhood. It is more common in men than women. The progression of LEMS depends on whether it occurs with cancer, although it is treatable in all its forms. LEMS that occurs in childhood is not associated with cancer.
MDA-supported scientists in countries around the world are working to reveal numerous facets of LEMS, from identifying possible causes and triggers  to the disease's molecular underpinnings to specific treatment strategies .
The first symptoms of LEMS are usually leg weakness and difficulty walking. Oculobulbar weakness (affecting the muscles of the eyes, face and throat) may occur later, causing ptosis (droopy eyelids), speech impairment and swallowing problems.
LEMS also sometimes causes autonomic (involuntary) symptoms such as dry mouth, constipation, impotence and bladder urgency.
In about 60 percent of cases, LEMS is associated with small-cell lung cancer (and more rarely with other types of cancer), which might be diagnosed at the same time as LEMS or years later.
There’s evidence that cancer cells inappropriately make a protein called voltage-gated calcium channel (VGCC), which triggers the immune system to make anti-VGCC antibodies. Some 85 to 90 percent of people with LEMS test positive for antibodies against VGCC, so even in cases where no cancer is present, LEMS can be confirmed by detection of anti-VGCC antibodies in the blood. For more on the molecular underpinnings of LEMS, see Causes/Inheritance .
The autonomic (involuntary) symptoms and predominant leg weakness of LEMS also help to distinguish it from myasthenia gravis (MG) . Electrodiagnostic testing that shows an increased muscle response to repeated stimulation also favors LEMS rather than MG (in which the response decreases).
|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 LEMS, they attack and damage muscle cells.|
The immune system normally defends the body against diseases, but sometimes it can turn against the body, leading to an autoimmune disease. LEMS is 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.
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.
While myasthenia gravis (MG)  targets the ACh receptors on muscle cells, LEMS interferes with ACh release from nerve cells.
Some 85 to 90 percent of people with LEMS test positive for antibodies against a protein called P/Q type voltage-gated calcium channel (VGCC). This protein is a pore that allows calcium entry into nerve cells, which is required for ACh release.
In cases where LEMS is associated with cancer, it's thought that the cancer cells inappropriately make VGCC, triggering the immune system to make anti-VGCC antibodies. The trigger for LEMS without cancer is unknown.
Long-term treatment and prognosis of LEMS depend on whether it occurs with or without cancer. Although cancer is life-threatening, it can be treated with radiation, surgery or chemotherapy. When these treatments are successful and the cancer goes into remission, LEMS usually goes into complete or partial remission as well.
Prior to cancer treatment, or in LEMS patients without cancer, immunosuppressant drugs, IVIg and/or plasmapheresis  often are helpful. More information about these treatments can be found on the Myasthenia Gravis Medical Management page .
Symptomatic relief can be achieved with Mestinon and/or 3,4-diaminopyridine (3,4-DAP), a drug that prolongs the opening of VGCC in nerve endings and thus enhances ACh release. This drug (3,4-DAP) may be hard to obtain, but you can ask about it through your MDA clinic  physician. It also may be available through research studies .
For more about Lambert-Eaton myasthenic syndrome management, see: Keeping Your Focus: Eye Care in Neuromuscular Disorders  and Not Always Smooth Sailing: Charting a corticosteroid course .
Today, the focus of MDA-supported research in Lambert-Eaton myasthenic syndrome, as it is for other autoimmune (self-immune) diseases, is largely on regulating the immune response.
Several research groups are working on rebalancing the errant immune system, so that it returns to a state where it is able to attack invading microbes but not the body's own tissues. One especially promising avenue in this regard is increasing the activity or numbers of so-called regulatory T cells, which can dampen an overactive, or misdirected, immune response.
For more details on the above, see New Directions: Can an immune response be rerouted to treat disease? 
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 LEMS 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.