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Home arrow Environment arrow Inflammatory Disorders of the Nervous System: Pathogenesis, Immunology, and Clinical Management
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Management

Management of MG should be individualized according to patient characteristics and the severity of the disease. There are two approaches for management of MG based on the pathophysiology of the disease. The first is by increasing the amount of ACh that is available to bind with the postsynaptic receptor using an acetylcholinesterase inhibitor agent, and the second is by using immunosuppressive medications that decrease the binding of acetylcholine receptors by antibodies.

There are four basic therapies used to treat MG:

  • 1. Symptomatic treatment with acetylcholinesterase inhibitors
  • 2. Rapid short-term immunomodulating treatment with plasma exchange (PE) and intravenous immunoglobulin (IVIg)
  • 3. Chronic long-term immunomodulating treatment with glucocorticoids and other immunosuppressive drugs
  • 4. Surgical treatment

Acetylcholinesterase Inhibitors

Acetylcholinesterase inhibitors are the first-line treatment in patients with MG. Response to treatment varies from marked improvement in some patients to little or no improvement in others. Acetylcholinesterase inhibitors are used as a symptomatic therapy and act by increasing the amount of available acetylcholine at the NMJ [46]. They do not alter disease progression or outcome. Pyridostigmine is the most commonly used drug. It has a rapid onset of action within 15 to 30 min, reaching peak activity in about 2 h. The effect lasts for about 3-4 h. The initial oral dose is 15-30 mg every 4-6 h and is titrated upwards depending on the patient’s response. Adverse side effects of pyridostigmine are mostly due to the cholinergic properties of the drug such as abdominal cramping, diarrhea, increased salivation and bronchial secretions, nausea, sweating, and bradycardia. Nicotinic side effects are also frequent and include muscle fasciculation and cramping. High doses of pyridostigmine exceeding 450 mg daily, administered to patients with renal failure, have been reported to cause worsening of muscle weakness [47].

 
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