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Myasthenia gravis
Myasthenia gravis is an autoimmune disease of the neuromuscular junction in which antibodies against the acetylcholine receptor cause weakness that worsens with effort and improves with rest — in the lids, eyes, swallowing and proximal muscles — with normal reflexes, sensation and pupils.
Why it matters in the exam
Questions present ptosis and double vision that worsen towards evening, trouble chewing and speaking, or shoulder weakness. They test the work-up (AChR and MuSK antibodies, repetitive nerve stimulation, single-fibre EMG, chest CT for thymoma), treatment (pyridostigmine, steroids and immunosuppressants, thymectomy), and recognising a myasthenic crisis with respiratory failure. An important part is the list of drugs that worsen myasthenia: aminoglycosides, fluoroquinolones, macrolides, magnesium and beta-blockers. A classic distractor is relying on normal oxygen saturation in a patient in crisis — breathing fails before saturation falls, so vital capacity is measured.
Key points
- Myasthenia is fatigable weakness of the lids, eyes, swallowing and proximal muscles, with normal pupils and sensation.
- Diagnosis by AChR or MuSK antibodies, repetitive nerve stimulation and single-fibre EMG; chest CT for every patient.
- Treatment: pyridostigmine, steroids and immunosuppressants, and thymectomy in AChR-positive disease at age 18 to 65.
- Crisis: measure vital capacity, give IVIG or plasma exchange, ventilate below 20 mL/kg.
- Aminoglycosides, fluoroquinolones, macrolides, magnesium and beta-blockers worsen myasthenia.
Summary table
| Topic | Core | Exam detail |
|---|---|---|
| Clinical picture | Fatigable weakness: ptosis, double vision, bulbar weakness, proximal weakness | Pupils, sensation and reflexes normal; the ice test improves ptosis |
| Diagnosis | AChR antibodies (most patients with generalised disease), MuSK antibodies; decrement on repetitive nerve stimulation; single-fibre EMG is the most sensitive | Chest CT for every patient — thymoma in about 10 to 15 percent |
| Symptomatic and immune treatment | Pyridostigmine; prednisone (start low and increase, because a high dose may cause early worsening); azathioprine or mycophenolate as steroid-sparing agents | Biologics: complement inhibitors (eculizumab) and FcRn blockers (efgartigimod) |
| Thymectomy | With thymoma — always; without thymoma — in generalised AChR-positive disease at age 18 to 65 | Reduces steroid need and improves the course |
| Myasthenic crisis | Respiratory or bulbar failure; intubate when vital capacity is below 20 mL/kg | IVIG 2 g/kg over 2 to 5 days or plasma exchange; hold pyridostigmine while ventilated |
A free exam question
בן ,60 מזה מספר חודשים סובל מפטוזיס, כפל ראיה, הפרעה בדיבור, בבליעה וחולשה בגפיים. בנוסף מתלונן על יובש בפה ובעיניים. התסמינים משתפרים במהלך היום. בבדיקה הנוירולוגית: רפלקסים לא מועיל Pyridostigmine -גידיים ירודים. טיפול ב. איזה נוגדנים פתולוגיים צפויים במקרה זה? (the question as examined, in Hebrew)
- א. Anti-acetylcholine receptor
- ב. Anti-Muscle Kinase
- ג. Anti-ryanodine
- ד. Anti-voltage gated calcium channels
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Sources
- International Consensus Guidance for Management of Myasthenia Gravis (Narayanaswami et al., Neurology), 2021 — Immunotherapy, thymectomy and crisis
- Thymectomy Trial in Non-Thymomatous Myasthenia Gravis (MGTX, NEJM), 2016 — Thymectomy in AChR antibody positive generalised disease
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.