Myasthenia Gravis (MG) is a chronic autoimmune disorder characterized by muscle weakness and paralysis, especially during sustained activity. The underlying cause of muscle paralysis in MG is linked to a defect at the neuromuscular junction, where nerve signals are transmitted to muscles.

Mechanism of Muscle Paralysis in Myasthenia Gravis

In MG, the body’s immune system produces antibodies against its own acetylcholine receptors (AChRs) located on the postsynaptic membrane of the neuromuscular junction. These antibodies either:

• Block the acetylcholine (ACh) binding sites on the receptors,

• Cause receptor degradation,

• Or interfere with the clustering and function of AChRs.

As a result, even though acetylcholine is released normally from nerve terminals, fewer functional receptors remain available to bind ACh. This leads to impaired neuromuscular transmission, resulting in progressive muscle weakness and episodes of paralysis.

Clarifying the Options

• (1) Failure of the nerve terminal to release acetylcholine is not the cause in MG. Acetylcholine release is typically normal.

• (2) Acetylcholine is not destroyed by acetylcholinesterase abnormally in MG; this enzyme functions normally.

• (3) The correct cause is that the patient develops antibody against his own acetylcholine receptor, reducing effective receptor numbers.

• (4) Antibodies against acetylcholine itself (the neurotransmitter) do not cause MG.

Conclusion

The correct answer is:

(3) The patient develops antibody against his own acetylcholine receptor.