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Myasthenia gravis

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Myasthenia Gravis Foundation of America diagnosis treatment patient information

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diagram normal and myasthenia gravis neuromuscular junction acetylcholine receptor antibodies

Myasthenia gravis (MG)

Myasthenia gravis is a chronic autoimmune disorder of the neuromuscular junction, the connection where nerves activate skeletal muscle. The immune system interferes with acetylcholine receptor signaling, causing fluctuating, fatigable muscle weakness. It is not contagious and does not affect sensation or cognition.

Typical symptoms

Weakness usually worsens with repeated activity and improves after rest:
  • Drooping eyelid (ptosis) and double vision
  • Facial weakness, altered speech, weak voice
  • Difficulty chewing or swallowing, especially late in meals
  • Neck, arm, or leg weakness
  • Shortness of breath in severe disease
Eye symptoms are often the first manifestation. Some people have disease confined to the eyes (ocular MG); others develop generalized weakness. Bradley and Daroff's Neurology in Clinical Practice, p. 1958.

Cause

Most cases involve antibodies against the acetylcholine receptor (AChR). Others involve MuSK or LRP4 antibodies, and some cases are antibody-negative on standard testing. These antibodies reduce effective nerve-to-muscle signaling. Goldman-Cecil Medicine, p. 4110-4111.
The thymus is relevant: thymic enlargement is common in some groups, and a thymoma is found in about 10% of patients. Therefore, chest imaging is generally part of the assessment. Goldman-Cecil Medicine, p. 4111.

Diagnosis

A neurologist typically diagnoses MG using:
  1. History and examination showing fatigable weakness
  2. Blood tests for AChR, MuSK, and sometimes LRP4 antibodies
  3. Nerve testing, especially repetitive nerve stimulation or single-fiber EMG
  4. Chest CT or MRI to assess the thymus
  5. Tests for associated autoimmune thyroid disease when appropriate
A negative antibody test does not completely exclude MG. The MGFA diagnostic overview describes how electrodiagnostic testing and the clinical picture are particularly important in seronegative disease.

Treatment

Treatment is individualized by symptoms, antibody type, disease severity, thymus findings, age, and pregnancy plans. Common options include:
  • Pyridostigmine for symptomatic improvement
  • Corticosteroids and steroid-sparing immunosuppressants for immune control
  • Thymectomy, mandatory for thymoma and beneficial for selected generalized AChR-antibody-positive patients
  • IVIG or plasma exchange for significant worsening, before surgery in selected cases, or myasthenic crisis
  • Targeted therapies for selected generalized MG, including complement inhibitors, neonatal Fc receptor blockers, and B-cell-directed treatments
The MGFA treatment guide summarizes these options. A recent systematic review documents the substantial quality-of-life burden of generalized MG (PMID: 38336636).

Myasthenic crisis: emergency

Seek emergency care immediately for:
  • Increasing breathlessness or inability to speak a full sentence
  • Trouble handling saliva, choking, or rapidly worsening swallowing
  • Rapidly progressive generalized weakness
  • Weak cough or inability to clear secretions
This can indicate myasthenic crisis, which may require hospital respiratory support and urgent treatment.

Practical points

Infections, surgery, fever, emotional stress, thyroid disease, and certain medications can worsen MG. Do not start or stop medicines without asking the clinician managing MG. In particular, medication choices such as some antibiotics, magnesium-containing products, and drugs that affect neuromuscular transmission may need special caution.
MG is often manageable, and many people achieve good symptom control with specialist care.
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