Which condition is characterized by antibodies against postsynaptic ACh receptors?

Myasthenia gravis is indeed characterized by the presence of antibodies against postsynaptic acetylcholine (ACh) receptors at the neuromuscular junction. This autoimmune condition leads to a decrease in the number of functional ACh receptors available for binding, resulting in impaired neuromuscular transmission. Patients typically experience muscle weakness that worsens with activity and improves with rest, a hallmark feature of the disease.

The key aspect of myasthenia gravis is that the body’s immune system mistakenly targets its own receptors, disrupting the normal process of muscle contraction. This results in varying degrees of muscular weakness, which may affect different muscle groups, including those controlling eye movements, facial expression, and limb strength.

Understanding the mechanism behind this condition involves recognizing that the antibodies block or destroy the receptors, preventing effective communication between nerves and muscles. This action contrasts with other neuromuscular disorders listed. For example, Lambert-Eaton myasthenic syndrome involves antibodies against presynaptic calcium channels, while paraneoplastic encephalomyelitis and Good syndrome involve different immune-mediated processes not directly targeting the ACh receptors. This clarification reflects the distinct pathophysiology that defines myasthenia gravis.