Synopsis
Recognise fatigable ocular, bulbar and limb weakness, detect myasthenic crisis before gas exchange fails, and coordinate antibody, thymus, symptomatic and immune treatment safely.
- Myasthenia gravis causes fluctuating, fatigable skeletal-muscle weakness that worsens with use and later in the day and improves with rest, while sensation and pupils remain normal.
- Ptosis and diplopia are common first features; variability between eyes and during sustained upgaze supports ocular fatigability but does not replace antibody and neurophysiology assessment.
- Bulbar disease causes nasal or slurred speech, chewing fatigue, nasal regurgitation, choking and weak cough and can progress to respiratory crisis without dramatic limb weakness.
- Test acetylcholine-receptor antibodies first in generalised or ocular disease, then MuSK and selected LRP4 or cell-based assays through specialist practice if seronegative.
- Repetitive nerve stimulation or single-fibre EMG demonstrates impaired neuromuscular transmission; routine nerve conduction and sensation are otherwise generally preserved.
- Image the mediastinum for thymoma in confirmed MG; thymectomy is required for thymoma and benefits selected non-thymomatous AChR-positive generalised disease.
- Pyridostigmine provides symptomatic improvement but can cause abdominal cramps, diarrhoea, sweating, salivation and, in excess, cholinergic weakness.
- Corticosteroids and steroid-sparing immunosuppression control generalised disease, but starting steroids can transiently worsen weakness and requires specialist timing and monitoring.
- In crisis secure ventilation and treat triggers, using IV immunoglobulin or plasma exchange for rapid immune effect; review antibiotics, magnesium, beta blockers and anaesthetic drugs that can worsen transmission.
Key red flags
Speech fading or becoming nasal, chewing failure late in meals, nasal regurgitation and choking indicate pharyngeal and facial weakness and aspiration risk.
Rapidly worsening cough, secretion handling, swallowing, neck flexion or breathing represents respiratory failure risk regardless of current oxygen saturation.
Prominent facial, neck, bulbar and respiratory weakness with relative limb sparing and limited pyridostigmine response raises MuSK-associated MG.
Worsening weakness accompanied by diarrhoea, abdominal cramps, salivation, sweating, bronchial secretions, bradycardia or miosis suggests excessive acetylcholinesterase inhibition.
Investigation priorities
Confirm autoimmune MG subtype and guide thymectomy, prognosis and treatment discussions.
Management branches
Variable ocular, bulbar or proximal weakness occurs without sensory loss.
- Examine ptosis, eye movements, speech, neck flexion and proximal power before and after safe sustained activity, documenting normal sensation, pupils and reflexes.
- Send AChR then MuSK or specialist antibodies and arrange repetitive stimulation or single-fibre EMG when required.
- Assess swallowing and respiratory symptoms immediately, admitting for progression rather than waiting for antibody results.
- After confirmation image the mediastinum, screen associated autoimmunity and refer to a neuromuscular service for subtype-specific treatment.