Myasthenia gravis

Last updated: September 11, 2023

Summarytoggle arrow icon

Myasthenia gravis (MG) is an autoimmune disease of the neuromuscular junction (NMJ) characterized by muscle weakness that worsens with activity and improves with rest. MG is caused by autoantibodies directed against postsynaptic molecules, most commonly acetylcholine receptors (AchR), resulting in impaired neuromuscular transmission. Women are more frequently affected; ∼ 10–15% of cases are associated with thymoma. The most common initial symptom is ocular muscle weakness (e.g., ptosis and/or diplopia), with progression to generalized weakness typically occurring within two years. The diagnosis is clinical and confirmed by antibody testing and electromyographic evaluation. Treatment of choice consists of acetylcholinesterase inhibitors; immunosuppressive drugs can be added if symptoms persist. All patients with MG should be screened for thymoma with CT chest. Thymectomy is indicated for patients with confirmed thymoma. Acute exacerbations, as seen in myasthenic crises, are generally treated with either IV immunoglobulins or plasma exchange.

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon


A minority of patients with myasthenia gravis have no detectable antibodies (i.e., seronegative MG). 100% of patients with thymoma have autoantibodies.

Associated conditions [3]

Classificationtoggle arrow icon

  • Ocular myasthenia: only the extraocular and/or eyelid muscles
  • Generalized myasthenia
    • All skeletal muscles may be involved.
    • Especially ocular, bulbar, limb, and respiratory muscles

Pathophysiologytoggle arrow icon

Thymus involvement

Acetylcholine receptor antibodies [4]

Clinical featurestoggle arrow icon

Symptoms [5]

Severity typically varies during the day and from day to day

Eye muscle involvement is the most common initial symptom in generalized disease; larger muscles are involved later in the disease course. [6]

Physical examination findings [5]

Physical examination may be completely normal in patients with myasthenia gravis, especially in mild cases.

  • Normal deep tendon reflexes
  • Limb weakness is typically symmetrical.
  • Ocular weakness (e.g., ptosis) is typically asymmetrical. [1]
  • Examination and proactive maneuvers can elicit typical ocular findings. [1]
    • The eyebrow of the unaffected eye is usually lower than the affected eyebrow. [5]
    • Ice-pack test: An ice pack placed on the affected eyelid for 5 minutes improves ptosis by ≥ 2 mm. [5][6]
    • Curtain sign: Lifting the more ptotic eyelid worsens ptosis in the contralateral eyelid; eyebrow elevation and furrowing of the forehead can also occur.
    • Cogan lid twitch sign: brief eyelid twitching when looking straight ahead after 10–20 seconds of downward gaze [5]
    • Simpson test: historically used to reproduce eyelid fatigue; positive if looking upward for > 1 minute (without lifting the head) provokes eyelid fatigue

Exacerbating factors of myasthenia gravis [7]

The following factors may worsen symptoms of MG and/or trigger a myasthenic crisis.

Diagnosticstoggle arrow icon

In patients with characteristic fatigable muscle weakness, confirm the diagnosis with serum auto-antibodies or; , if negative, by electromyography (EMG). [5]

Laboratory studies [5][6]

Results can confirm the diagnosis and be used to classify MG into subgroups depending on the antibody profile.

Consider diagnostic studies for other autoimmune disorders (e.g., Hashimoto thyroiditis, rheumatoid arthritis, SLE) in patients with suggestive symptoms.

Additional studies [5][6]

  • EMG of affected muscles ; [5]
  • Chest CT: indicated in all patients with confirmed myasthenia gravis to assess for a thymoma or thymic hyperplasia
  • Edrophonium test: administration of a rapid-acting, short-duration acetylcholinesterase inhibitor to assess for symptom improvement in patients with suspected myasthenia gravis
    • Historically used to diagnose myasthenia gravis; currently replaced by the more specific and sensitive anti-AChR antibody test
    • No longer available in the U.S.

The edrophonium test was discontinued by the FDA in 2018 because of high false-positive rates.

Differential diagnosestoggle arrow icon

Lambert-Eaton myasthenic syndrome (LEMS) [9]

Comparison of Myasthenia gravis and LEMS

Myasthenia gravis vs. Lambert-Eaton myasthenic syndrome
Myasthenia gravis Lambert-Eaton myasthenic syndrome
Associated diseases
  • Starts with weakness of proximal limb muscles
  • Improves with exercise and throughout the day
  • Normal
  • Reduced or absent
Repetitive nerve stimulation
  • Decremental response
  • Incremental response
Autonomic dysfunction
  • None
  • Common
Response to cholinesterase inhibitors
  • Symptomatic relief
  • No response

Other differential diagnoses

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

General principles

  • For patients with MG and difficulty breathing, admit to the hospital to rule out or treat myasthenic crisis.
  • Provide supportive therapy and avoid exacerbating factors for myasthenia gravis.
  • Treatment aims to control symptoms but is not curative.
    • Titrate pharmacotherapy to minimize adverse effects, usually in consultation with a neurologist.
    • Refer for thymectomy based on disease subtype and adequacy of pharmacological symptom management.

Supportive therapy [5]

Avoid the use of muscle relaxants, fluoroquinolones, macrolides, and aminoglycosides in patients with myasthenia gravis because of the risk of worsening muscle weakness. [12]


Glucocorticoids may be a part of the management of myasthenia gravis; however, caution is required as they have been associated with myasthenic crises in 9–18% of patients, especially within the first two weeks of initiating treatment. [7][12]

Thymectomy [5]

  • Consider for:
    • Most patients with thymoma, based on surgical risk factors and adequacy of medical management
    • Select patients without thymoma in whom immunotherapy is not successful or not tolerated
  • Potential benefits include:
    • Reduced symptoms and exacerbations
    • Decreased doses of pharmacotherapy

Patients with rare subtypes of MG (e.g., MuSK-Ab) generally do not benefit from thymectomy. [12]

Complicationstoggle arrow icon

Myasthenic crisis [6][7]

∼ 60–90% of patients with myasthenic crises require intubation with mechanical ventilation. Elective intubation is preferred over emergent intubation. [7]

Differential diagnosis of myasthenic crisis and cholinergic crisis

Myasthenic crisis vs. cholinergic crisis
Myasthenic crisis Cholinergic crisis
Shared symptoms
  • Normal
  • None
  • Present
Heart rate
  • Cold and faint
  • Warm and flushed
Bronchial secretion
  • Normal
  • Increased

We list the most important complications. The selection is not exhaustive.

Prognosistoggle arrow icon

  • The prognosis of ocular MG is good.
  • Mortality
    • Without treatment: up to 30%
    • With treatment: less than 5%

Special patient groupstoggle arrow icon

Myasthenia gravis during pregnancy [14]

  • Risk of developing myasthenia gravis is increased in pregnant and postpartum individuals.
  • Myasthenic symptoms often worsen during pregnancy, most commonly during the first trimester.
  • Pregnant individuals are at increased risk of myasthenic crisis.
  • Cesarean sections are commonly required for pregnant patients with MG because of ineffective contractions due to muscle weakness and risk of exhaustion during vaginal delivery.
  • In about 10% of cases, newborns develop transient neonatal myasthenia (due to the transfer of maternal antibodies), which usually manifests with swallowing and sucking difficulties.

In the case of preeclampsia, individuals with myasthenia gravis should not be treated with magnesium sulfate since it worsens myasthenia symptoms.

Referencestoggle arrow icon

  1. Gilhus NE. Myasthenia Gravis Can Have Consequences for Pregnancy and the Developing Child. Frontiers in Neurology. 2020; 11.doi: 10.3389/fneur.2020.00554 . | Open in Read by QxMD
  2. Gilhus NE. Myasthenia Gravis. N Engl J Med. 2016; 375 (26): p.2570-2581.doi: 10.1056/nejmra1602678 . | Open in Read by QxMD
  3. Asmail A, Kesler A, Kolb H, Drory VE, Karni A. A tri-modal distribution of age-of-onset in female patients with myasthenia gravis is associated with the gender-related clinical differences. Int J Neurosci. 2018; 129 (4): p.313-319.doi: 10.1080/00207454.2018.1529669 . | Open in Read by QxMD
  4. Priola AM, Priola SM. Imaging of thymus in myasthenia gravis: From thymic hyperplasia to thymic tumor. Clin Radiol. 2014; 69 (5): p.e230-e245.doi: 10.1016/j.crad.2014.01.005 . | Open in Read by QxMD
  5. Romi F, Aarli JA, Gilhus NE. Seronegative myasthenia gravis: disease severity and prognosis. European Journal of Neurology. 2005; 12 (6): p.413-418.doi: 10.1111/j.1468-1331.2005.01137.x . | Open in Read by QxMD
  6. Gilhus NE, Tzartos S, Evoli A, Palace J, Burns TM, Verschuuren JJGM. Myasthenia gravis. Nat. Rev. Dis. Primers. 2019; 5 (1).doi: 10.1038/s41572-019-0079-y . | Open in Read by QxMD
  7. Gwathmey K, Burns T. Myasthenia Gravis. Semin Neurol. 2015; 35 (04): p.327-339.doi: 10.1055/s-0035-1558975 . | Open in Read by QxMD
  8. Wendell LC, Levine JM. Myasthenic Crisis. Neurohospitalist. 2011; 1 (1): p.16-22.doi: 10.1177/1941875210382918 . | Open in Read by QxMD
  9. Romi F. Thymoma in Myasthenia Gravis: From Diagnosis to Treatment. Autoimmune Diseases. 2011; 2011: p.1-5.doi: 10.4061/2011/474512 . | Open in Read by QxMD
  10. Kesner VG, Oh SJ, Dimachkie MM, Barohn RJ. Lambert-Eaton Myasthenic Syndrome. Neurol Clin. 2018; 36 (2): p.379-394.doi: 10.1016/j.ncl.2018.01.008 . | Open in Read by QxMD
  11. Mareska M, Gutmann L. Lambert-Eaton Myasthenic Syndrome. Semin Neurol. 2004; 24 (02): p.149-153.doi: 10.1055/s-2004-830900 . | Open in Read by QxMD
  12. Anwar A, Saleem S, Ahmed MF, Ashraf S, Ashraf S. Recent Advances and Therapeutic Options in Lambert-Eaton Myasthenic Syndrome. Cureus. 2019.doi: 10.7759/cureus.5450 . | Open in Read by QxMD
  13. Narayanaswami P, Sanders DB, Wolfe G, et al. International Consensus Guidance for Management of Myasthenia Gravis. Neurology. 2020; 96 (3): p.114-122.doi: 10.1212/wnl.0000000000011124 . | Open in Read by QxMD
  14. Mehta S. Neuromuscular disease causing acute respiratory failure. Respir Care. 2006; 51 (9): p.1016-21; discussion 1021-3.
  15. Waterman SA. Autonomic dysfunction in Lambert-Eaton myasthenic syndrome. Clinical Autonomic Research. 2001; 11 (3): p.145-154.doi: 10.1007/bf02329922 . | Open in Read by QxMD

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