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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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| 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 |
| 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 |
| 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 |

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 |