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SHARE: Lambert-Eaton Myasthenic Syndrome
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            What is Lambert-Eaton myasthenic syndrome?

Lambert-Eaton myasthenic syndrome (LEMS) is a disorder of the neuromuscular junction—the place where nerve and muscle cells meet to help activate a person's muscles. LEMS is caused by a disruption of electrical impulses between the two kinds of cells.

LEMS is an autoimmune condition. Normally, the body's immune system protects the body from infection and disease. In autoimmune conditions, the immune system attacks the body's own tissues by mistake.

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Learn About Clinical Trials

Clinical trials are studies that allow us to learn more about disorders and improve care. They can help connect patients with new and upcoming treatment options.

How can I or my loved one help improve care for people with Lambert-Eaton myasthenic syndrome?

Consider participating in a clinical trial so clinicians and scientists can learn more about the LEMS and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat, or prevent disease.

All types of volunteers are needed—those who are healthy or may have an illness or disease—of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.

For information about participating in clinical research visitNIH Clinical Research Trials and You. Learn about clinical trials currently looking for people with LEMS atClinicaltrials.gov.

Where can I find more information about Lambert-Eaton myasthenic syndrome?

The following resource may help:

Genetic and Rare Diseases (GARD) Information Center
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The NINDS Publication Catalog offers printed materials on neurological disorders for patients, health professionals, and the general public. All materials are free of charge, and a downloadable PDF version is also available for most publications. Health Information
  
    

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      Last reviewed on November 28, 2023
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