Introduction

Myasthenia gravis is an autoimmune disease in which antibodies are produced that block or destroy the nicotine acetylcholine receptors at the postsynaptic membrane, causing muscle weakness and fatigue (Pendleton & Schultz-Krohn, 2006). Myasthenia gravis can occur at any age but onset usually occurs at an earlier age in women than in men. In the United States, there are about 14.2 cases of myasthenia gravis per one million people (Pendleton & Schultz-Krohn, 2006).
Myasthenia gravis will be discussed in this paper according to the following: etiology, signs and symptoms, pathology and the progression of myasthenia gravis, diagnosis, prognosis, medical interventions, complications and resulting dysfunction of myasthenia gravis.
Etiology
Romi, Gilhus, and Aarli (2005) point to a genetic predisposition for myasthenia gravis with 30% of patients having mothers with myasthenia gravis or another autoimmune disease (p. 136). Other precipitating factors may include surgery, certain drugs, infection, and disorders of the thymus (Beers & Porter, 2006, p. 1899). Approximately 12% of babies born to mothers with myasthenia gravis display a passing muscle weakness termed “neonatal myasthenia” (Keesy, 2004, p. 485) not considered autoimmune, due to maternal antibodies crossing the placenta. Myasthenia gravis occurs at any age with the peak onset age in males between 50 and 70 years and in females between the teens and the thirties. Both sexes display a bimodal curve with a clear early-onset group and a late-onset group (Keesy, 2004, p. 485). Different sites at the neuromuscular junction are implicated. At pre-synaptic sites, acetylcholine packaging or synthesis may be defective. Nerve impulses may also release deficient quantities of acetylcholine or quantal without synaptic vesicles. At synapses, there may be a deficiency in endplate acetylcholinesterase. Post-synaptic sites may show a decrease in acetylcholine response because of a mutation in receptor subunits, a deficiency in plectrin, receptor clustering due to rapsyn mutations, or an increased response to acetylcholine resulting in slow-channel syndrome (Keesy, 2004, p. 485). 75-90% of patients are seropositive for acetylcholine receptor antibodies that bind to acetylcholine receptors. 10-25% of seronegative patients have been found to carry a different antibody, now identified as anti-muscle specific kinase antibodies, that bind to tyrosine kinase receptors on the muscle side of the neuromuscular junction (Keesy, 2004, p. 486). Myasthenia gravis affects people in many different ways and it is important to know that every patient may present with different signs and symptoms of the disease. At one time the individual may function normally, and at another time he or she may experience severe loss of strength. Most patients with the disease begin to have symptoms of weakness in muscles that control the eye or eyelids. The symptoms range from difficulty in eye motion resulting in double vision or droopy eyelids on one or both sides. The symptoms may progress in any number of ways. 10 to 20% of people who present with ocular symptoms have symptoms remain long term and never have symptoms progress to other parts of their body (Goodman et al., 2003).
The other group of patients with ocular symptoms may experience spontaneous improvement, however within the first year of diagnosis there is a chance that they will experience some kind of fluctuation of the illness. These patients may have symptoms other than ocular manifestations such as oral symptoms including difficulties with swallowing, chewing, speaking, smiling, and breathing (Goodman et al., 2003). Within the first year, patients with ocular symptoms may experience weakness and numbness throughout the body with feelings of heaviness, muscular spasm, or loss of limb control. Limb weakness often presents asymmetrically. Myasthenia gravis is in itself painless, but the strain of supporting weak limbs or the neck can be painful. Additionally, patients with muscle weakness may experience a sense of loss of balance (Goodman et al. , 2003). A diagnosis of myasthenia gravis can have an impact on a person’s daily routines. Patients can experience problems with vision, muscle weakness, and fatigue. They may also have difficulty swallowing, chewing, and breathing (Leonardi, Raggi, Antozzi, Confalonieri, Maggi, Cornelio, & Mantegazza, 2009). As mentioned, myasthenia gravis is a fluctuating disorder and repetitive muscle movement can cause a decrease in muscle strength and endurance by the end of the day (Pendleton & Schultz-Krohn, 2006, p. 943).
According to Adams (2008), there are other situations that can intensify the resulting dysfunction of myasthenia gravis, such as stress, pregnancy, heat, and certain medications. Some patients with myasthenia gravis also experience benign tumors called thymomas. Removing the tumor depends on the situation of each patient, such as their age, and the degree of their myasthenia gravis (Gilhus, 2009). Additionally, patients may reach myasthenic crisis, which is a sudden worsening of diaphragmatic muscle strength that impairs breathing. A patient who is in myasthenic crisis may go into respiratory collapse if untreated (Kothari, 2004). Because of the complicated etiology and fluctuating nature of symptoms, patients are often referred to the neurology departments at major medical centers or to neuromuscular disease specialists. The Myasthenia Gravis Foundation of America provides patients with resources and information about the disease and research continues with the hope of an eventual cure.

References
Adams, A. (2008). Mayo clinic essential neurology. Rochester, MN: Mayo foundation for medical reasearch.
Beers, M. H., & Porter, R. S. (Eds.). (2006). Section 16 Neurologic disorders. In The
Merck manual of diagnosis and therapy (18th ed., pp. 1899-1901). Whitehouse Station, NJ: Merck Research Laboratories.
Gilhus, N. E. (2012). Autoimmune myasthenia gravis. Expert Review of Neurotherapeutics, 9(3), 351-362. http://dx.doi.org/10.1586/14737175.9.3.351
Goodman, C.C., Boissonnault, W.G., & Fuller, K. S. (2003). The peripheral nervous system. In Pathology: Implication for the physical therapist (2 ed., pp. 1167-1172). Philadelphia, Pennsylvania: Saunders.
Keesey, J. C. (2004). Clinical evaluation and management of myasthenia gravis. Muscle and Nerve, 29, 484-505.
Kothari, M. J. (2004). Myasthenia gravis. The Journal of the American Osteopathic Association, 104(9), 377-384. Retrieved from http://www.jaoa.org/content/104/9/377.full
Leonardi, M., Raggi, A., Antozzi, C., Confalonieri, P., Maggi, L., Cornelio, F., &
Mantegazza, R. (2009). Identification of international classification of functioning, disability and health relevant categories to describe functioning and disability of patients with myasthenia gravis. Disability and Rehabilitation, 31(24), 2041-2046.
Owe, J.F., Daltveit, A.K., & Gilhus, N. E. (2006). Causes of death among patients with myasthenia gravis in Norway between 1951 and 2001. Journal of Neurology, Neurosurgy and Psychiatry, 77(2): 203–207. Retrieved from doi: 10.1136/jnnp.2005.072355
Pendleton, H. M., & Schultz-Krohn, W. (2006). Disorders of the motor unit. In Pedretti's occupational therapy: Practice skills for physical dysfunction (pp. 943-945). St. Louis, MO: Elsevier/Mosby.
Raggi, A., Leonardi, M., Antozzi, C., Confalonieri, P., Maggi, L., Cornelio, F., & Mantegazza, R. (2010). Concordance between severity of disease, disability and health-related quality of life in myasthenia gravis. Neuorological Sciences, 31(1), 41-45. http://dx.doi.org/10.1007/s10072-009-0167-y
Romi, F., Gilhus, N. E., & Aarli, J. A. (2005). Myasthenia gravis: Clinical, immunological, and therapeutic advances. Acta Neurologica Scandinavica, 111, 134-141. doi: 10.1111/j.1600-0404.2005.00374.x