Myasthenia gravis
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Myasthenia gravis
Myasthenia Gravis (MG) is a chronic neuromuscular disorder that leads to the weakness of skeletal muscles. Skeletal muscles control and facilitate functions such as breathing and movement of body parts such as legs and arms. The disorder arises when there is an impairment of communication between muscles and nerve cells. MG is a common neuromuscular communication disorder. The condition is relatively rare in the United States and affects about 14 to 20 people in every 100 000 people.
Causes
The condition is commonly caused by the autoimmune problem. Autoimmune conditions arise when the immune system mistakenly acts on healthy body tissue. The disorder is caused due to an occurrence of an error in the nerve impulses transmissions to muscles. It arises when there is an interruption of normal communication between nerve and muscle at the neuromuscular junction. The neuromuscular junction is a point where nerve cells link with their associated muscles. Neurons and brain cells communicate information by using neurotransmitters chemicals. Generally, an acetylcholine transmitter is released when impulses (electrical signals) move down a motor nerve. Acetylcholine binds the muscle sites called acetylcholine receptors. Muscle contraction is activated when acetylcholine binds to its receptor (NHS, 2019).
Antibodies in myasthenia gravis cause blockage, alteration, and destruction of acetylcholine receptors at the neuromuscular junction, which prevents muscle contraction. This is caused by acetylcholine receptor antibodies and other proteins like muscle-specific kinase (MuSK). It might damage transmission at the neuromuscular junction.
Symptoms
The commons symptom is a general weakness of skeletal muscles. It occurs as a result of their inability to respond due to nerve impulses. Muscle and nerve communication is blocked, leading to muscle weaknesses. The symptom worsens due to increased physical activity while it improves due to rest. There are several other symptoms, which include: fatigue, double vision, trouble while talking, facial paralysis, hoarse voice, drooping eyelids, swallowing and chewing difficulties, breathing difficulties, and difficulties while lifting objects or walking upstairs.
Diagnoses
Blood tests- acetylcholine receptor antibodies levels are abnormally elevated in individuals with MG. Also, the Blood test detects the acetylcholine receptor antibodies.
Diagnostic imaging- Thymoma presence is detected by the diagnostic chest imaging using either CT (computed tomography) or MRI (magnetic resonance imaging).
Pulmonary function testing- measure breathing strength to forecast whether a respiratory failure can cause myasthenic crises.
An edrophonium test- it used edrophonium injections to temporarily relieve myasthenia gravis weaknesses in people. It blocks acetylcholine breakdown to raise its levels at the neuromuscular junction. Usually, it is used for testing ocular muscle weakness.
Electrodiagnostics test- involve repetitive stimulation of nerves with small electric pulses to tire certain muscles. In Myasthenia Gravis and other neuromuscular disorders, muscle fibers do not respond well to when they are electrically repeatedly stimulated than other muscles form healthy people. EMG (electromyography) is of significance in the diagnoses of myasthenia gravis mild cases where the alternative test does not reveal abnormalities.
Physical and neurological examination- an individual medical history is reviewed by a physician then a physical examination is conducted. The neurological examination involves inspection of muscle strength and tone
Treatment
The condition of the disorder can be improved by the reduction of muscle weaknesses. There are various therapies which include thymectomy, monoclonal antibody, anticholinesterase medications, immunosuppressive drugs, and intravenous and plasmapheresis immunoglobulin (Tanden et al. 2017).
Thymectomy- is an operation where the thymus gland is removed to lessen symptoms as well as curing some patients through immune system rebalancing.
Monoclonal antibody- the treatment approach targets the process through which acetylcholine antibodies in the neuromuscular junction are injured.
Immunosuppressive drugs- suppresses the production of abnormal antibodies leading to muscle improvement. Some of the medication include tacrolimus, mycophenolate mofetil, azathioprine, and prednisone
Anticholinesterase medications- they improve muscle strength as well as neuromuscular transmission by breaking down acetylcholine at the neuromuscular junction. Some of the drugs used in the medication include anticholinesterase agents like pyridostigmine and Mestinon.
Intravenous and plasmapheresis immunoglobulin- are alternatives in cases where myasthenia gravis is severe. Antibodies in the plasma in some affect the neuromuscular junction. The treatments work by getting rid of destructive antibodies. Plasmapheresis procedure involves the use of a machine to get rid of destructive antibodies present in plasma. They are replaced by either plasma substitute or a good plasma. Intravenous immunoglobulin involves the injection of highly concentrated antibodies obtained from healthy donors to change the working of the immune system. It binds with harmful antibodies and eventually removes them from the circulatory system.
Neuromuscular junction homeostatic synaptic plasticity
The neuromuscular junction is a site located between muscle fiber and motor neurons. At the site, low-density lipoprotein receptor, extracellular protein matrix, and muscle-specific tyrosine kinase are needed for complex differentiation as well as alignment of structure. Synaptic plasticity is the overtime changes of synaptic strength. It regulates the communication between two neurons. Synaptic strength changes in keeps on changing over time.
In Myasthenia gravis synaptic transmission is disrupted due to postsynaptic acetylcholine receptors attack. Synaptic strength is controlled in a homeostatic manner to ensure the safety of motor neuron muscle transmission during different conditions. The blockage of action potentials entering the presynaptic nerve terminal is triggered by Myasthenia Gravis. It occurs due to nerves Na channels blockage. Nerve and muscle are silenced by the manipulation. Presynaptic action potential blockage triggers the release of more acetylcholine from the synaptic vesicles. The quantal content increases due to the blockage of action potentials. Also, an homeostatic regulation can occur due to the blockage of postsynaptic receptors instead of action potentials (Wang & Rich, 2017). The spontaneous synaptic currents decrease as a result of the immune attack as well as blockage of acetylcholine.
Myasthenia gravis complications
Myasthenic crises are the most dangerous complication. It comprises the life-threatening weakness of vial muscles, which can lead to breathing difficulties. Moreover, myasthenia gravis exposes patients to lupus and rheumatoid arthritis autoimmune disorders.
Research areas
There is research on the development of better medication, identification of new diagnoses techniques as well as treatment, and treatment improvement alternatives. Medication- some MG patients do not respond well to the available treatment options. Currently, there is the testing of new drugs in a move to come up with better medications. Diagnostics and biomarkers- there is research on better treatment and diagnosis techniques. New treatment techniques- there are trials about the benefits of surgical procedures for people who do not have thymoma.
Myasthenia is a rare condition, but it is important for people to have knowledge about it. The information is applicable as well as important in the healthcare setting. The diagnosis and treatment information can be used in healthcare with respect to the identification of the best treatment and diagnosis alternatives.
References
Tandan, R., Hehir, M. K., Waheed, W., & Howard, D. B. (2017). Rituximab treatment of myasthenia gravis: a systematic review. Muscle & nerve, 56(2), 185-196.
NHS. Overview – Myasthenia Gravis. 2019, www.nhs.uk/conditions/myasthenia-gravis/.
Wang, Xueyong, and Mark M. Rich. “Homeostatic Synaptic Plasticity at the Neuromuscular Junction in Myasthenia Gravis.” Annals of the New York Academy of Sciences, vol. 1412, no. 1, 5 Oct. 2017, pp. 170–177, 10.1111/nyas.13472. Accessed 6 Nov. 2019.