Myasthenia gravis is an autoimmune disease that prevents proper conduction of impulses at the neuromuscular junction of voluntary muscles. The immune system produces defective antibodies that bind to receptor sites at the neuromuscular junction usually reserved for the neurotransmitter acetylcholine (Conti-Fine 2006). In individuals with myasthenia gravis, up to 80% of these sites can be taken up by antibodies. Because these sites are already occupied, acetylcholine is unable to play its part in the transmission of the nerve impulse to the muscle. This ultimately leads to muscle weakness, the hallmark symptom of myasthenia gravis (Trouth 2012). According to the Myasthenia Gravis Fact Sheet, “Certain muscles such as those that control eye and
