History of MG

MG Information > History of MG

We think that MG has always been with us but one of the earliest descriptions was recorded in 1672 by Dr Thomas Willis, a well known London physician, who wrote: “…in the mornings, they are able to walk firmly…. Or to take up any heavy thing. Before noon, the stock of the spirits being spent, which had flowed into the muscles, they are scarce able to move hand or foot….A prudent and honest woman has this spurious palsie since many years, not only in her members (limbs)…. But, after she has spoke long, hastily or eagerly, she becomes as mute as a fish; nor can she recover the use of her voice under an hour or two…
Does this sound familiar to you?

From that time until the 19th century, progress was slow, apart from the fact that in Germany around 1860 the distinction between Motor Neurone Disease (MND) and MG was made. Unlike MND, MG was not regarded as remorselessly progressive but that the disease was fatigable. That is the harder one tried the weaker they became.

In France, in 1850, research on the South American arrow poison Curare showed that it created conditions similar to MG in that it blocked the activation of the muscles. When an antidote for Curare was developed from the Calabar bean poison the way was paved for the production of Physostigmine. The modern Neuromuscular Blocking Agents (see above in Drugs Not to Have with Myasthenia) are derivatives of curare. An early test for myasthenia used an injection of a very small amount of curare that had no effect on normal individuals but made myasthenics markedly worse, although hopefully they survived the test.

MG was first named Myasthenia Gravis or Grave Muscle Weakness about 1895. (prior to modern understanding of the disorder and treatments)

Then in 1934 a young hospital doctor in England, Mary Walker, thought that patients with myasthenia looked like patients who had been given too much curare. She tried the antidote for curare, pyridostigmine, on a patient with myasthenia who had a quick and remarkable improvement. She was subsequently involved in developing the oral equivalent: Mestinon.

Both Curare and Quinine, which is also produced from the bark of the rain forest trees, were used in diagnosis because they both exacerbated the MG symptoms. As you can imagine, this was very dangerous.

In America improved anaesthetics made the removal of the Thymus Gland possible when tumours had been identified. It was discovered that some patients with MG and Thymoma greatly improved following this surgery. This led to the practice of removing the Thymus Gland for MG patients even when no tumour was present resulting in significant improvement in the condition of some.

In 1973 scientists experimenting with snake venom to purify the ACh Receptors in electric fish were able to prove conclusively that MG could be caused by antibodies. This became a valuable diagnostic tool which is used throughout the world today.

The understanding of the role of the antibodies led to the use of plasma exchange (plasmapheresis), where about four litres of the patient’s blood is drained a litre at a time and placed in a centrifuge and the plasma, where the antibodies are found, removed. The plasma is replaced by fresh plasma, leading to a lowering of the antibody level. This procedure is particularly useful where respiratory crisis situations exist, until other treatments become effective or where surgery is planned on a very weak patient. It is only effective for up to approximately four weeks.

A recent feature in the history of MG has been the increased incidence of older women being diagnosed. This has been observed in WA and in other parts of Australia, and studies in the Scandinavian Countries have confirmed this to be a world wide modern day phenomena. No definite reason has yet been advanced except that people are living longer.

Not all of the women, when tested, prove antibody positive and in most cases the Thymus gland is no longer active. It has been established that in a number of such patients a protein presence has been found at the neuromuscular junctions which has been given the name Muscle Specific Tyrosine Kinase (MuSK).