Neuromuscular Signaling in Myasthenia Gravis [MG] Patients

Myasthenia gravis (MG) is one of the most common disorders of neuromuscular signaling, with a prevalence of 13 to 21 per 100,000 in the United States. The symptoms experienced by people with MG include muscle weakness and generalized fatigue. In healthy patients, the presynaptic terminals release acetylcholine (ACH) from the motor nerve terminal in quanta, which then diffuse across the synaptic cleft and connect to receptors on the post synaptic membrane of the muscle, resulting in membrane depolarization and muscle contraction. In MG patients, however, the post synaptic ACH membrane receptors are destroyed or damaged mostly due to immunological or genetic abnormalities. Thymic tumors are also commonly seen in patients with MG. In MG, immune system B‐cells interact with helper T‐cells to produce antibodies to the ACH receptors. The destruction of the thymic tolerance can cause or contribute to an immune attack on the ACH receptors. MG can often be treated with cholinesterase inhibitors such as neostigmine bromide or thymectomy to enhance the diminished hormone‐ligand interaction needed to effect depolarization and muscle contraction. The current study utilized a Meta‐analysis approach for data interpretation in order to compare neuromuscular signaling in MG patients who were treated with cholinesterase inhibitors versus those who were treated surgically. Furthermore, this study intends to show that neuromuscular signaling in MG patients who have had surgical interventions tend to have more favorable outcomes than those treated with cholinesterase inhibitors alone. In our studies we also included noninvasive biophotonic diagnostic and electroceutical neuromuscular stimulation as alternative diagnostic and therapeutic measures with good success. Support or Funding Information Supported by Institutional resources of USAT College of Medicine and the Einstein Medical Institute