APEA Neurology Practice Test

The key idea is that acetylcholinesterase inhibitors improve muscle strength in myasthenia gravis. In MG, antibodies reduce the number or function of acetylcholine receptors at the neuromuscular junction, so transmission is weak and fatigable weakness occurs. When you give an acetylcholinesterase inhibitor, acetylcholine is increased in the synaptic cleft, temporarily enhancing receptor activation and strengthening the muscle response. This pharmacologic response—improved weakness after AChE inhibition—has historically been used to support a MG diagnosis and guides therapy with drugs like pyridostigmine. Immunoglobulin therapy, while important for crisis management or perioperative care, is not a diagnostic or hallmark pharmacologic response. Worsening after acetylcholinesterase inhibitors is not characteristic of MG and would prompt consideration of other issues such as a cholinergic crisis or different neuromuscular disorder.