A 26-year-old man comes to the emergency department because of progressive weakness and double vision for 2 days.

He reports difficulty climbing stairs and says his eyelids “feel heavy” by evening. Symptoms improve after rest. He recently recovered from a respiratory infection. Physical examination shows bilateral ptosis and proximal muscle weakness. Deep tendon reflexes are normal. Sensation is intact.

Which of the following is the most likely underlying mechanism of this patient’s condition?

A. Autoantibodies against presynaptic voltage-gated calcium channels

B. Destruction of dopaminergic neurons in the substantia nigra

C. Antibody-mediated destruction of postsynaptic acetylcholine receptors

D. Demyelination of peripheral nerves by macrophages

E. Mutation in dystrophin gene causing muscle fiber degeneration

Answer

C. Antibody-mediated destruction of postsynaptic acetylcholine receptors

Explanation

This patient has classic features of Myasthenia Gravis:

fluctuating muscle weakness,

ptosis and diplopia,

worsening with activity,

improvement with rest,

normal reflexes and sensation.

The disease is caused by autoantibodies targeting postsynaptic nicotinic acetylcholine receptors at the neuromuscular junction.

Why the other choices are wrong

A → Lambert-Eaton Myasthenic Syndrome causes proximal weakness that improves with use and often decreased reflexes.

B → Parkinson Disease causes tremor, rigidity, bradykinesia.

D → Guillain-Barré Syndrome presents with ascending weakness and reduced reflexes.

E → Duchenne Muscular Dystrophy presents in childhood with Gowers sign and calf pseudohypertrophy.