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.
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.
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.
Key medicines
Pyridostigmine bromideOften start 30 mg four times daily and titrate timing and dose, commonly to 60 mg four times daily, within specialist and BNF limits.
PrednisoloneUse a neuromuscular-specialist low-start or inpatient regimen with gradual titration and taper chosen according to bulbar, respiratory and disease severity.