Acetylcholinesterase inhibitors can provide symptomatic benefit and may not fully remove a person's weakness from MG.  While they might not fully remove all symptoms of MG, they still may allow a person the ability to perform normal daily activities.  Usually, acetylcholinesterase inhibitors are started at a low dose and increased until the desired result is achieved. If taken 30 minutes before a meal, symptoms will be mild during eating, which is helpful for those who have difficulty swallowing due to their illness. Another medication used for MG, atropine , can reduce the muscarinic side effects of acetylcholinesterase inhibitors.  Pyridostigmine is a relatively long-acting drug (when compared to other cholinergic agonists), with a half-life around four hours with relatively few side effects.  Generally, it is discontinued in those who are being mechanically ventilated as it is known to increase the amount of salivary secretions.  A few high-quality studies have directly compared cholinesterase inhibitors with other treatments (or placebo); their practical benefit may be such that it would be difficult to conduct studies in which they would be withheld from some people.  The steroid prednisone might also be used to achieve a better result, but it can lead to the worsening of symptoms for 14 days and takes 6–8 weeks to achieve its maximal effectiveness.  Due to the myriad symptoms that steroid treatments can cause, it is not the preferred method of treatment.  Other immune suppressing medications may also be used including rituximab .  About 10% of people with generalized MG are considered treatment-refractory. 
Myasthenia gravis is an autoimmune disorder, which occurs when the immune system malfunctions and attacks the body's own tissues and organs. In myasthenia gravis , the immune system disrupts the transmission of nerve impulses to muscles by producing a protein called an antibody that attaches (binds) to proteins important for nerve signal transmission. Antibodies normally bind to specific foreign particles and germs, marking them for destruction, but the antibody in myasthenia gravis attacks a normal human protein. In most affected individuals, the antibody targets a protein called acetylcholine receptor (AChR); in others, the antibodies attack a related protein called muscle-specific kinase (MuSK). In both cases, the abnormal antibodies lead to a reduction of available AChR.