Essay --

Historically, Myasthenia Gravis was discovered by Thomas Willis in 1672. It was not until late 19th century that Wilhelm Erb and Samuel Goldflam described the muscle disease due the lack of nervous input. Initially, it was called the Erb-Goldflam syndrome until Friedrich Jolly, a German neurologist coined it as Myasthenia Gravis Pseudoparalytica. He created the Jolly test, which tested for muscle weakness by eliciting faradic stimulations for continuous muscular contractions that caused fatigue (Ropper & Samuels 2009). Myasthenia Gravis (MG) is an autoimmune disease that causes antibodies to destroy the signal transduction in neuromuscular transmission. In an autoimmune disease such as myasthenia Gravis, the immune system cannot differentiate between healthy cells and antigens. The host’s antibodies block the acetylcholine nicotinic receptors resulting in inhibition of the excitatory effects of the neurotransmitter acetylcholine. It also degrades the acetylcholine receptors. Normally, the antibodies do not attack normal healthy acetylcholine receptors on the postsynaptic end of the neuromuscular junction. Acetylcholine is released from the vesicles from the presynaptic end into the synaptic cleft where it binds to the acetylcholine nicotinic receptors eliciting an excitatory effect for muscle contraction. Once this action is inhibited, muscle contraction in that cell cannot be elicited. These nicotinic acetylcholine receptors are found on the motor end plate of the muscle cell. Acetylcholine binding 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 to power stroke causing the cell to contract (Ropper & Samuels 2009). Myasthenia Gra... ...l lives. In conclusion, immunosuppressive agents and acetylcholinesterase inhibitors help in reducing the symptoms of Myasthenia Gravis. While acetylcholinesterase inhibitors have a short half-life accompanied by various side effects, it is the best solution at this time to alleviate muscle weakness and fatigue. Pyridostigmine is the most commonly used drug with the lowest toxicity amongst these inhibitors because of its limited bioavailability. Immunosuppressive drugs inhibit antibody release reducing the amount of malfunctioning T-cells that attack the nicotinic acetylcholine receptors. While its effects are not immediate with poor absorption, it provides longer periods of symptom relief. The immunological agents are only reduced and not destroyed and thus regenerate to elicit myasthenic symptoms. Further research is necessary to continue the search for a cure.