surgical method to treat mg. medication neostigmine, chemical structure azathioprine, chemical structure worsening may occur with medication such as fluoroquinolones, aminoglycosides, and magnesium. about 10% of people with generalized mg are considered treatment-refractory. autologous hematopoietic stem cell transplantation (hsct) is sometimes used in severe, treatment-refractory mg. available data provide preliminary evidence that hsct can be an effective therapeutic option in carefully selected cases. efgartigimod alfa was approved for medical use in the united states in december 2021. acetylcholinesterase inhibitors 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 so significant that conducting studies in which they would be withheld from some people would be difficult. immune suppressants the steroid prednisone might also be used to achieve a better result, but it can lead to the worsening of symptoms and takes 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 or azathioprine. plasmapheresis and ivig if the myasthenia is serious (myasthenic crisis), plasmapheresis can be used to remove the putative antibodies from the circulation. also, intravenous immunoglobulins (ivigs) can be used to bind the circulating antibodies. both of these treatments have relatively short-lived benefits, typically measured in weeks, and often are associated with high costs, which make them prohibitive; they are generally reserved for when mg requires hospitalization. surgery as thymomas are seen in 10% of all people with the mg, they are often given a chest x-ray and ct scan to evaluate their need for surgical removal of their thymus glands and any cancerous tissue that may be present. even if surgery is performed to remove a thymoma, it generally does not lead to the remission of mg. surgery in the case of mg involves the removal of the thymus, although in 2013, no clear benefit was indicated except in the presence of a thymoma. a 2016 randomized, controlled trial, however, found some benefits. physical measures people with mg should be educated regarding the fluctuating nature of their symptoms, including weakness and exercise-induced fatigue. exercise participation should be encouraged with frequent rest. in people with generalized mg, some evidence indicates a partial home program including training in diaphragmatic breathing, pursed-lip breathing, and interval-based muscle therapy may improve respiratory muscle strength, chest wall mobility, respiratory pattern, and respiratory endurance. medical imaging in people with myasthenia gravis, older forms of iodinated contrast used for medical imaging have caused an increased risk of exacerbation of the disease, but modern forms have no immediate increased risk. prognosis the prognosis of people with mg is generally good, as is quality of life, when given very good treatment. monitoring of a person with mg is very important, as at least 20% of people diagnosed with it will experience a myasthenic crisis within two years of their diagnosis, requiring rapid medical intervention. generally, the most disabling period of mg might be years after the initial diagnosis. in the early 1900s, 70% of detected cases died from lung problems; now, that number is estimated to be around 3–5%, an improvement attributed to increased awareness and medications to manage symptoms. epidemiology mg occurs in all ethnic groups and both sexes. it most commonly affects women under 40 and people from 50 to 70 years old of either sex, but it has been known to occur at any age. younger people rarely have thymoma. prevalence in the united states is estimated at between 0.5 and 20.4 cases per 100,000, with an estimated 60,000 americans affected. in the united kingdom, an estimated 15 cases of mg occur per 100,000 people. history the first to write about mg were thomas willis, samuel wilks, erb, and goldflam. the term "myasthenia gravis pseudo-paralytica" was proposed in 1895 by jolly, a german physician. mary walker treated a person with mg with physostigmine in 1934. simpson and nastuck detailed the autoimmune nature of the condition. in 1973, patrick and lindstrom used rabbits to show that immunization with purified muscle-like acetylcholine receptors caused the development of mg-like symptoms. research immunomodulating substances, such as drugs that prevent acetylcholine receptor modulation by the immune system, are currently being researched. some research recently has been on anti-c5 inhibitors for treatment research as they are safe and used in the treatment of other diseases. ephedrine seems to benefit some people more than other medications, but it has not been properly studied as of 2014. in the laboratory, mg is mostly studied in model organisms, such as rodents. in addition, in 2015, scientists developed an in vitro functional, all-human, neuromuscular junction assay from human embryonic stem cells and somatic-muscle stem cells. after the addition of pathogenic antibodies against the acetylcholine receptor and activation of the complement system, the neuromuscular co-culture shows symptoms such as weaker muscle contractions.