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Neurology›Condition·Updated Apr 17, 2026·v1

Myasthenia Gravis

Myasthenia gravis is an antibody-mediated autoimmune disorder of the neuromuscular junction causing fatigable muscle weakness. Diagnosis relies on serology (AChR/MuSK antibodies) and electrophysiology, while management involves acetylcholinesterase inhibitors, immunosuppressants, and thymectomy.

High Evidence88 references·492 words·2 min read·v1
NeurologyNeuromuscular JunctionAutoimmuneMyasthenia Gravis

Quick Reference

RxDrug of choicePyridostigmine (symptomatic); Prednisone (immunosuppressive)
AltAlternativesAzathioprine, Mycophenolate mofetil, Efgartigimod, Eculizumab
⊘AvoidMagnesium sulfate, Aminoglycosides, Telithromycin, Fluoroquinolones
DxTest of choiceAChR-antibody serology (initial); SFEMG (most sensitive)
ScKey scoreMG-ADL (Activities of Daily Living) and QMG (Quantitative MG) score
→When to referAll new diagnoses for specialist neurology evaluation; immediately for any bulbar or respiratory symptoms
MG is a treatable NMJ disorder defined by fatigable weakness; management requires balancing symptomatic relief, long-term immunosuppression, and vigilance for respiratory crisis.
Myasthenia gravis (MG) is the most common primary disorder of neuromuscular transmission, characterized by fluctuating skeletal muscle weakness and pathological fatigability. This autoimmune condition is caused by antibodies directed against components of the postsynaptic membrane at the [[neuromuscular junction]], most frequently the acetylcholine receptor (AChR). The clinical hallmark is diurnal variation, where symptoms are typically mild or absent in the morning but worsen following repetitive activity or toward the end of the day.

Overview and Recommendations

Background

  • •Recognize myasthenia gravis as a chronic of the characterized by a bimodal age distribution. Early-onset disease predominantly affects women in their 20s and 30s, while late-onset disease (LOMG) is increasingly diagnosed in patients over age 65, often presenting with more severe initial symptoms and higher comorbidity burdens.
  • •Understand the primary pathophysiology involving pathogenic autoantibodies that interfere with synaptic transmission. Approximately 80% of generalized MG patients possess antibodies against the acetylcholine receptor (AChR-Ab), while 5-8% have antibodies against muscle-specific kinase (MuSK-Ab), which often correlates with a more severe bulbar and respiratory phenotype.
  • •Identify the critical role of the thymus gland in disease pathogenesis. Thymic hyperplasia is common in early-onset AChR-positive cases, while —a primary thymic epithelial tumor—is present in approximately 10-15% of all MG patients and necessitates oncological evaluation.
  • •Screen for common triggers that can induce new-onset disease or precipitate exacerbations. These include viral infections (notably ), physiological stress, surgery, and specific medications such as , immune checkpoint inhibitors (ICIs), and certain antibiotics.
  • •Note the clinical variants, including (OMG), where symptoms are restricted to the extraocular muscles. Approximately 40% of patients with OMG will progress to generalized myasthenia gravis (gMG) within two years of symptom onset.

Evaluation

  • •Suspect myasthenia gravis in any patient presenting with fluctuating ptosis, diplopia, slurred speech, or proximal limb weakness that worsens with use. Ask specifically about diurnal variation—symptoms that are better after a night's sleep or a nap but progress throughout the afternoon.
  • •Perform a fatigability examination by asking the patient to maintain an upward gaze for 60 seconds to elicit ptosis or to count aloud from 1 to 100 to detect progressive dysarthria or a nasal quality to the voice.
  • •Utilize the ice pack test at the bedside for patients with ptosis; application of an ice pack to the affected eyelid for 2 minutes that results in ≥2 mm of improvement is highly suggestive of MG due to the temperature sensitivity of acetylcholinesterase.
  • •Order serum autoantibody testing as the initial diagnostic step. Obtain AChR-binding, blocking, and modulating antibodies; if negative and the clinical suspicion for generalized MG is high, reflex to MuSK-Ab and LRP4-Ab testing.
  • •Perform repetitive nerve stimulation (RNS) in a weak muscle, looking for a >10% decremental response in the compound muscle action potential (CMAP) at low-frequency (2-3 Hz) stimulation.
  • •Request single-fiber electromyography (SFEMG) if serology is negative but clinical suspicion remains high. This is the most sensitive diagnostic test for MG, showing increased 'jitter' or impulse blocking, though it is technically demanding and less specific than antibody testing.
  • •Obtain a CT or MRI of the chest in all newly diagnosed patients to rule out , regardless of the severity of symptoms or antibody status.
  • •Evaluate respiratory mechanics immediately if the patient reports dyspnea or exhibits bulbar weakness. Measure the Forced Vital Capacity (FVC) and Maximal Inspiratory Pressure (MIP); an FVC < 15 mL/kg or MIP < -30 cmH2O indicates an impending crisis.
  • •Rule out mimics such as (characterized by autonomic dysfunction and strength that improves with exercise) and (characterized by loss of deep tendon reflexes and ascending paralysis).
  • •Assess for the 'curtain sign' during the ocular exam: manually lifting the more ptotic eyelid may cause the contralateral eyelid to droop further, demonstrating the shared neural drive (Hering's Law) and compensatory effort.

Management

  • •Administer Pyridostigmine 60 mg orally every 4 to 6 hours as the first-line symptomatic treatment for most patients. Adjust the dose based on clinical response and tolerance of cholinergic side effects like abdominal cramping or diarrhea.
  • •Initiate Prednisone 0.5 to 1.0 mg/kg/day for patients who remain symptomatic on pyridostigmine. Start at a low dose (e.g., 10-20 mg/day) and titrate upward slowly to avoid the transient 'steroid flare'—a paradoxical worsening of weakness that can occur in the first two weeks of high-dose therapy.
  • •Introduce steroid-sparing agents such as Azathioprine 2-3 mg/kg/day or Mycophenolate mofetil 1000 mg twice daily for long-term maintenance. Counsel patients that these agents may take 6 to 12 months to reach full clinical efficacy.
  • •Refer for in patients aged 18-65 with AChR-positive generalized MG. Surgical removal of the thymus increases the probability of remission and reduces the long-term requirement for corticosteroids.
  • •Manage an impending myasthenic crisis (IMC) with rapid-acting immunomodulation. Administer Efgartigimod 10 mg/kg IV weekly for 4 weeks; this FcRn antagonist rapidly reduces IgG levels and has shown superior early improvement compared to traditional therapies.
  • •Utilize Intravenous Immunoglobulin (IVIg) 2 g/kg divided over 2 to 5 days or Plasmapheresis (PLEX) for 5 to 7 exchanges as alternative rescue therapies for acute exacerbations or as a preoperative bridge.
  • •Escalate to C5 inhibitors such as Eculizumab or Ravulizumab for patients with refractory AChR-positive generalized MG who fail conventional immunosuppression.
  • •Avoid medications known to exacerbate neuromuscular blockade. Strictly contraindicated or high-risk drugs include Magnesium sulfate, aminoglycosides (e.g., Gentamicin), fluoroquinolones (e.g., Ciprofloxacin), and beta-blockers.
  • •Monitor respiratory status closely during exacerbations. Do not rely solely on oxygen saturation; intubate electively if the patient develops severe dysphagia (bulbar failure) or if the FVC drops below 15 mL/kg to prevent aspiration and sudden respiratory arrest.
  • •Maintain a 'Nothing by Mouth' (NPO) status for any patient with a Quantitative Myasthenia Gravis (QMG) bulbar subscore ≥2 to prevent , which is a leading cause of mortality in myasthenic crisis.
  • •Transition pregnant patients to the safest possible regimen. Use Pyridostigmine and Prednisone as first-line; avoid Mycophenolate and Methotrexate due to teratogenicity. Be prepared for transient neonatal myasthenia in 10-20% of newborns due to maternal antibody transfer.

Board Review — High Yield

  • •Cogan's lid twitch — Brief overshoot of the upper eyelid when shifting gaze from downward to primary position.
  • •MuSK-positive MG — Often presents with severe bulbar/respiratory weakness and may be worsened by Pyridostigmine.
  • •Thymoma — Found in 10-15% of MG; requires surgical resection regardless of MG severity.
  • •Ice pack test — Positive if ptosis improves by ≥2mm after 2 minutes of cooling (inhibits acetylcholinesterase).
  • •Myasthenic Crisis — Respiratory failure requiring mechanical ventilation; usually triggered by infection or medication changes.
  • •Decrement on RNS — A >10% drop in CMAP amplitude between the 1st and 4th/5th stimuli at 2-3 Hz.
  • •Hering's Law of Equal Innervation — Explains the 'curtain sign' where lifting one eyelid worsens ptosis in the other.
  • •Transient Neonatal MG — Occurs in 10-20% of infants born to MG mothers; caused by passive transfer of IgG antibodies.

Deep Dive — Evidence Details

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