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Myasthenia Gravis

Autoimmune Neuromuscular Junction Disorder Causing Fluctuating Muscle Weakness with Fatigability

Written by: Saygı Hospital Health Guide Editorial Board
Last updated:

This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

References (5)

This content is for informational purposes only and does not constitute medical advice. You can book an appointment at our Nöroloji department. Book Appointment →

What is Myasthenia Gravis?

Myasthenia gravis (MG) is a chronic autoimmune disorder of the neuromuscular junction caused by antibodies against postsynaptic acetylcholine receptors (AChR), MuSK or LRP4; prevalence 70–200 per million.

Pathophysiology: autoantibodies attack the neuromuscular junction (most commonly anti-AChR antibodies, 80–85%), reducing functional acetylcholine receptors and impairing neuromuscular transmission; complement-mediated postsynaptic membrane damage.

Subtypes: ocular MG (limited to ocular muscles, 15%), generalized MG (most common form), thymoma-associated MG (10–15%), congenital myasthenic syndromes (rare, genetic), neonatal MG (transient maternal antibody transfer).

Bimodal age distribution: early onset (under 50, female predominance) and late onset (over 50, male predominance with thymoma association).

Symptoms

Fluctuating muscle weakness with fatigability — hallmark feature (worsens with use, improves with rest)
Ocular symptoms (50–60% initial presentation): ptosis (drooping eyelids), diplopia (double vision), variable extraocular muscle involvement
Bulbar symptoms (15%): dysarthria, dysphagia, weak chewing, nasal regurgitation, dysphonia
Limb weakness: proximal more than distal, affecting arms more than legs (difficulty raising arms, climbing stairs)
Neck weakness: head drop, especially after prolonged activity
Respiratory weakness: shortness of breath on exertion, orthopnea, sleep apnea, myasthenic crisis with respiratory failure
Diurnal variation: symptoms worse at end of day, better in morning
Worsening with: heat, illness, stress, pregnancy, certain medications (aminoglycosides, beta-blockers, magnesium, neuromuscular blockers)
Myasthenic crisis: rapid worsening of generalized and respiratory weakness, requires intensive care and intubation

Risk Factors

Female sex (early-onset MG, 2:1 female:male)
Age 20–40 years (early-onset) or >50 years (late-onset)
Genetic predisposition: HLA-B8, HLA-DR3 alleles in early-onset
Thymic abnormalities: thymic hyperplasia (60–80% in early-onset), thymoma (10–15%)
Other autoimmune diseases: thyroid disease, type 1 diabetes, rheumatoid arthritis, lupus
Family history of myasthenia gravis or autoimmune disease
Recent infection (URI, viral illness)
Stress, pregnancy, surgery (potential triggers)
Certain medications (penicillamine, interferon-alpha, immune checkpoint inhibitors)

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • New ptosis or diplopia, especially fluctuating
  • Difficulty chewing, swallowing or speech changes
  • Weakness worsening with exertion or end of day
  • Difficulty raising arms above head, climbing stairs
  • Nasal regurgitation of liquids, choking on food
  • Shortness of breath, especially when supine (urgent)
  • Recently diagnosed with worsening or new symptoms
  • Myasthenic crisis suspicion: rapid weakness, breathing difficulty (urgent)

Treatment Methods

01
Diagnostic workup: detailed history (fluctuating weakness pattern), neurological examination with fatigability testing, ice pack test for ptosis
02
Antibody testing: anti-AChR antibodies (80–85% sensitivity in generalized MG), anti-MuSK (5–10%), anti-LRP4 (1–3%); seronegative in 5–10% of cases
03
Electrodiagnostic testing: repetitive nerve stimulation (decremental response >10% at 3 Hz, sensitivity 60–70%), single-fiber EMG (sensitivity 95–99%)
04
Edrophonium (Tensilon) test: rare currently due to side effects; rapid response with edrophonium 2–10 mg IV
05
Imaging: chest CT to evaluate thymus for thymoma or hyperplasia in all newly diagnosed adult patients
06
Acetylcholinesterase inhibitors (first-line symptomatic): pyridostigmine 30–120 mg every 4–6 hours; titrate to symptoms; side effects include diarrhea, abdominal cramps, sweating
07
Corticosteroids: prednisolone 1 mg/kg/day initially with gradual escalation to avoid worsening; long-term use 5–20 mg/day; consider for moderate-to-severe disease
08
Steroid-sparing immunosuppression: azathioprine (2–3 mg/kg/day), mycophenolate mofetil (2–3 g/day), methotrexate (15–25 mg/week), cyclosporine, tacrolimus
09
Plasmapheresis: 5 sessions over 1–2 weeks for myasthenic crisis or severe exacerbation; rapid onset, short duration of effect (4–6 weeks)
10
Intravenous immunoglobulin (IVIg): 2 g/kg over 2–5 days; for myasthenic crisis or severe disease; equivalent efficacy to plasmapheresis but easier administration
11
Eculizumab (anti-C5 complement inhibitor): for refractory generalized AChR-positive MG; significantly improves quality of life and functional outcomes
12
Efgartigimod (FcRn antagonist): reduces circulating IgG levels; for refractory AChR-positive generalized MG
13
Ravulizumab and zilucoplan: complement inhibitors for refractory AChR-positive disease
14
Rozanolixizumab: FcRn antagonist for AChR or MuSK-positive disease
15
Thymectomy: improves outcomes in non-thymomatous AChR-positive MG (MGTX trial); essential in thymoma; ideally within 1–3 years of diagnosis
16
Myasthenic crisis management: ICU admission, mechanical ventilation, plasmapheresis or IVIg, hold acetylcholinesterase inhibitors, treatment of underlying trigger (infection, medication)
17
Cholinergic crisis (rare): excessive AChE inhibitor; muscarinic symptoms (sweating, miosis, salivation, cramps); treat by stopping AChE inhibitor
18
Pregnancy considerations: most medications safe (pyridostigmine, prednisolone), avoid mycophenolate, methotrexate; thymectomy not during pregnancy; close neurological monitoring
19
Avoid medications: aminoglycosides, fluoroquinolones, macrolides, beta-blockers, calcium channel blockers, magnesium, neuromuscular blockers
20
Vaccination: avoid live vaccines on immunosuppression; pneumococcal, influenza, COVID-19 vaccines safe and recommended
21
Long-term outcomes: 80–90% of patients achieve clinical remission or minimal symptoms with appropriate treatment; 5-year survival >95%; quality of life largely preserved
22
Multidisciplinary follow-up: neurology, immunology, thoracic surgery (for thymectomy), pulmonology (for crisis management), physical therapy, occupational therapy, psychology

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