Multiple Sclerosis and Myasthenia Gravis

Multiple sclerosis (MS) and myasthenia gravis (MG) can both cause weakness, but the weakness behaves differently because the injured structures are different. MS affects the central nervous system. Immune-mediated inflammation damages myelin and can produce axonal or neuronal loss, leaving lesions distributed across the brain, optic nerves, brainstem, cerebellum, and spinal cord. The clinical picture therefore depends on which CNS pathways are affected. Visual loss, sensory change, limb weakness, spasticity, ataxia, tremor, bladder dysfunction, and cognitive symptoms may occur in different combinations. The disease may follow a relapsing or progressive course; older labels such as relapsing-remitting, secondary progressive, and primary progressive describe the course but do not replace current diagnostic criteria. MG affects the postsynaptic neuromuscular junction. Autoantibodies most commonly target the acetylcholine receptor (AChR); some patients have antibodies against muscle-specific tyrosine kinase (MuSK). The nerve impulse arrives, but transmission across the junction becomes unreliable, especially after repeated use. Ptosis, diplopia, dysarthria, dysphagia, neck flexion weakness, and proximal limb weakness become more pronounced with activity and improve after rest. That contrast is clinically useful: a persistent sensory or visual deficit...