Historically, myasthenia gravis was discovered by Thomas Willis in 1672. It was not until the late 19th century that Wilhelm Erb and Samuel Goldflam described the muscle disease due to lack of nerve input. Initially, it was called Erb-Goldflam syndrome until Friedrich Jolly, a German neurologist, coined it as Myasthenia Gravis Pseudoparalytica. He created the Jolly test, which tests for muscle weakness by eliciting faradic stimulation for continuous muscle contractions that cause fatigue (Ropper & Samuels 2009). Myasthenia gravis (MG) is an autoimmune disease that causes antibodies to disrupt signal transduction in neuromuscular transmission. In an autoimmune disease such as myasthenia gravis, the immune system cannot distinguish between healthy cells and antigens. Host antibodies block nicotinic acetylcholine receptors resulting in inhibition of the excitatory effects of the neurotransmitter acetylcholine. It also degrades acetylcholine receptors. Normally, antibodies do not attack the normal healthy acetylcholine receptors on the postsynaptic end of the neuromuscular junction. Acetylcholine is released from vesicles from the presynaptic tip into the synaptic cleft where it binds to nicotinic acetylcholine receptors causing an excitatory effect for muscle contraction. Once this action is inhibited, muscle contraction in that cell cannot be stimulated. These nicotinic acetylcholine receptors are found on the endplate of the muscle cell. The binding of acetylcholine allows a cascade of events to release calcium into the muscle cell. This allows the movement of actin and myosin based on the sliding filament theory for a power stroke that causes the cell to contract (Ropper & Samuels 2009). Myasthenia Gra...... center of paper ...... l lives. In conclusion, immunosuppressive agents and acetylcholinesterase inhibitors help reduce the symptoms of myasthenia gravis. Although acetylcholinesterase inhibitors have a short half-life accompanied by various side effects, at this time they are the best solution for relieving muscle weakness and fatigue. Pyridostigmine is the most commonly used drug with the lowest toxicity among these inhibitors due to its limited bioavailability. Immunosuppressant drugs inhibit the release of antibodies by reducing the amount of malfunctioning T cells that attack nicotinic acetylcholine receptors. Although its effects are not immediate and have poor absorption, it provides longer periods of symptom relief. Immunological agents are only reduced and not destroyed and then regenerate to elicit myasthenic symptoms. More research is needed to continue the search for a cure.