Treatment:
Click this to see an example of the tests that neurologists complete to determine the severity of MG. These scores have a direct effect on treatment decisions.
Current Treatments:
The treatments currently available for MG take different approaches and can be used in various combinations. The treatment and dosage depend largely on the severity of the disease, which is determined by serum antibody counts and quantitative neurological exams. Click the link to the right to see the score sheet and test that is completed.[1] Below are the currently available treatments.
Cholinesterase Inhibitors: As explained in the physiology portion of this site, acetylcholine (Ach) is released into the synaptic cleft and binds to receptors on the postsynaptic membrane. Ach is degraded by its enzyme, acetylcholinesterase. That is where these medications take action. The cholinesterase inhibitors, inhibit the acetylcholinesterase, which allows Ach to remain active for a longer time period. Although this does not stop the immune response against the Ach receptors, it allows the active receptors to remain active longer. This reduces the muscle weakness.[2] Below are some examples of cholinesterase inhibitors, routes and doses from myasthenia.org.[1]
Corticosteriods: These drugs are thought to have an effect on MG through immune suppression. Prednisone is the most commonly used corticosteroid. It is thought to decrease the activation of T cells, limited the autoimmune activity. These are typically used as a short term solution and can exacerbate the symptoms of MG at first. There are long term side effects depending on the dose and longevity of use.[3]
Immunomodulatory Treatment: Two types of treatment are used in this case. The first is the use intravenous immunoglobin (IVIg). This comes from the blood of donors and works on the immune system response to MG through decreasing the life time of the IgG antibodies released by the B cells in the autoimmune response of MG. This can treat the underlying cause of autoimmunity in MG and has shown improvement in 70% of cases [Kim]. The second is through plasma exchange. In short plasma exchange allows the purification of the patient's plasma and quick removal of many immune system components that lead to and are causing the autoimmune response.[4]
Thymectomy: The last current treatment we will discuss is thymectomy. As discussed in the clinical repercussions of this site, thymoma can occur in MG. The thymectomy involves the removal of the thymoma and/or part of or all of the thymus. There are debates on the exact connection of the thymus to MG, but studies have shown that removal tends to reduce symptoms. In some cases, the procedure is completed regardless of whether or not a thymoma is present. Overall, this has shown a decrease in symptoms.[5] To the right is a diagram of this procedure.
Figure 1: This table shows commonly used cholinesterase inhibitors, their routes and dosages.
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Current Research for Treatments:
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Lewis describes the new and upcoming treatments associated with MG and the focus on the underlying factors that contribute to the autoimmune response of MG. He discusses the ability to target B cells to reduce the antibodies being produced, the reduction of B cell activating factor to decrease the ability to activate the B cell, therapies to target the complement response caused by the antibodies and the targeting of T-cell activation, migration and proliferation using various drugs.[6]
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Specifically, Robeson et al. is trying a new drug related approach to solving the autoimmune response in MG. They are studying the use of rituximab, a monoclonal antibody. This reduces the B cell antibodies and the study shows that clinical remission can be acheived up to 56 weeks after treatment and B cell antibody decrease.[7]
