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Myasthenia gravis (MG) is a chronic autoimmune neuromuscular junction disorder characterized by fluctuating skeletal muscle weakness and fatigability, most commonly caused by autoantibodies against acetylcholine receptors (AChR) or muscle-specific kinase (MuSK).

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Pathophysiology


Mechanism Effect
Anti-AChR antibodies (85%) Block or destroy acetylcholine receptors at the neuromuscular junction
Anti-MuSK antibodies (~5–8%) Disrupt clustering of AChRs
Anti-LRP4 and seronegative MG (<5%) Other autoimmune variants
Thymus abnormalities (hyperplasia or thymoma) Contribute to autoantibody production

Epidemiology


Feature Details
Bimodal age peak Young women (2nd–3rd decade), older men (6th–8th decade)
Sex Female predominance in early-onset, male in late-onset
Incidence ~10–20 per 100,000 persons

Clinical Features


Symptoms Description
Ocular symptoms (most common) Ptosis and diplopia (initial in ~60% of cases)
Bulbar symptoms Dysarthria, dysphagia, nasal speech
Limb weakness Proximal > distal, worsens with exertion
Respiratory involvement Can lead to myasthenic crisis (life-threatening)
Fatigability Hallmark; improves with rest
No sensory or reflex deficits Distinguishes from neuropathies

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Types of MG

Type Description
Ocular MG Limited to eye muscles
Generalized MG Involves bulbar, limb, and respiratory muscles
Neonatal MG Transient, passive transfer of antibodies from mother
Congenital MG Genetic, not autoimmune; rare

Radiology