Grave Muscle Weakness

In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring.

Normally, when impulses travel down the nerve, the nerve endings release a neurotransmitter substance called acetylcholine.
- Is caused by the presence of antibodies to the Ach receptor.
- Is characterized by skeletal muscle weakness and fatigability resulting from a reduced number of ACh receptors on the muscle end plate.
- The size of EPP is reduced; therefore, it is more difficult to depolarize the muscle membrane to threshold and to produce action potentials.
- Treatment with AChE inhibitors prevents the degradation of ACh and prolongs the action of ACh at the muscle end plate, partially compensating for the reduced number of receptors.
- Myasthenia gravis is characterized by a decreased density of acetylcholine (ACh) receptors at the muscle end plate.  An acetylcholinesterase (AChE) inhibitor blocks degradation of ACh in the neuromuscular junction, so levels at the muscle end plate remain high, partially compensating for the deficiency of receptors.

- Antibodies against nicotinic acetylcholine receptors cause myasthenia gravis.


Reference:
1. Ganong's Review of Medical Physiology: 23rd Edition.  Kim E. Barrett et al.  McGraw-Hill Publishing. 2010.