Myasthenia Gravis

If acetylcholine is not liberated than it would also not cause an action potential which would not cause a muscle contraction.

Some of the general symptoms of the disease can be characterized by hind limb spasticity, weight loss, tremors, abnormal posture with lordosis, and possibility of visual impairment. Muscle weakness, clasping of the limbs, and myoclonic twitches of the head that can be onset late in the disease. Research of the GM2 ganglioside has revealed that storage of the fatty substance varies a large

Guillain-Barre Syndrome (GBS) is a rare autoimmune disease. This is where an individual’s own immune system attacks and destroy healthy body tissue. The exact cause of this syndrome is unknown. However, once triggered the immune system begins to attack the myelin sheath in the brain, particularly, your peripheral nervous system (PNS). The PNS connects the brain and spinal cord (central nervous system – CNS) to the rest of the body. The myelin sheath main function is to ensure fast propagation of nerve impulses. When damaged it can often result in muscle weakness or paralysis.

Myasthenia Gravis is a disease that happens due to a receptor protein resting on top of muscle cells (Stanfield, C, 2017). This receptor ends up gaining control of groups of acetylcholine receptors that are needed for normal function (Stanfield, C, 2017). By disrupting that normal function is causes the muscle to not function at an optimal level. The way that this disease is tested is by taking blood samples to observe antibodies acting against the acetylcholine receptor (Stanfield, C, 2017). This test was done on Annie which showed that she contracted this disease in addition to her

Myasthenia Gravis(MG) is an auto immune disorder characterized by sudden dysarthria, which affects muscles that help produce speech, causing difficultly to pronounce words. But other symptoms include, droopy eye lids, muscle weakness and difficulty swallowing. Because of the sudden dysarthria, many elderly people are being misdiagnosed for possible strokes. Due to the great extent of the misdiagnoses of MG, researchers did a study presenting four subjects that had been presented to the ER with history of hypertension and sudden onset dysarthria. After considering the patients in each study, researchers found that all patients were initially misdiagnosed and treated for strokes, therefore prolonging the correct diagnose of MG and the correct form of treatment for these patients. Once each patient

Myasthenia gravis (MG) is an autoimmune disease that affects nerve impulses to skeletal muscles. There are varying types of this disease and the symptoms can range from mild, a person having peripheral skeletal muscle weakness, to severe, a person having breathing problems (Sieb, 2014). Myasthenia gravis is diagnosed in 20 out of 100,000 people in the United States, and women are more likely than men to have the disease (Meriggioli and Sanders, 2012). This autoimmune disease can happen at any age, but women generally have an earlier onset than men; the mean age for females is 28 and 42 for males (Nair, Patil-Chhablani, Venkatramani, and Gandhi 2014). To better understand this disease this

The cause of Stiff-Person Syndrome is still unknown it is believed that since there are

Involvement of muscles in neurological disease has been extensively studied over the past century. By 1830, Charles Bell had identified muscular dystrophy as a cause of progressive weakness among boys (McConville & Vincent, 2002). After extensive research, it was established that the disorder was of neurological origin. Together with other diseases such as Myasthenia gravis, Parkinson disease among others, it has been determined that muscular involvement in these diseases arises from the neuromuscular connection. More importantly, many neural transmissions occur at the muscle junctions through the actions of neurotransmitters. Any changes in the amount or structural defects of the synapse cause muscular weakness and gradually loss of function. In other severe cases, loss of nerves at the junctions causes permanent disability since nerves cannot be regenerated. This focus will examine existing literature to provide an association of muscles properties and neurological involvement.

Myasthenia gravis can be classified as a chronic neurologic disease of the neuromuscular transmission and characterized by presentation of fatigable muscle weakness to the external ocular, cranial, respiratory and limb muscles (Smith, C., P.A.-C., & Stickler, D., M.D. 2012). The incidence of this disease is about 20 per 100,000 people in various populations, affecting mostly women in their 20’s to 30’s and men over the age of 60 (Postevka 2013).

Nicotinic acetylcholine receptors are receptor proteins that respond to the neurotransmitter acetylcholine. They are widely expressed in the central nervous system of humans, playing important roles in the peripheral nervous system.

Hypokalemic periodic paralysis is a medical emergency leading to muscle paralysis. Among the hypokalemic periodic paralysis,familial hypokalemic periodic paralysis (FPP)is the most common cause in Western countries,and Thyrotoxic periodic paralysis (TPP), characterized by the triad of acute hypokalemia without total body potassium deficit, muscle paralysis, and thyrotoxicosis, is the most common cause in Asia. Although cases with TPP are mostly uniformly males of Asian descent, cases have been reported in persons of Polynesian, African, Hispanic, Greek, and American Indian descent.

Damage to the neuromuscular junctions is due to an autoimmune disease called myasthenia graves. The motor end plates, which are located on skeletal muscles, are affected because there is a decrease in the amount of Ach receptors located on the motor end plate, which is connected to the neuromuscular junction. The decrease is due to the unnecessary production of antibodies, which bind to the motor end plate. This prevents Ach from binding to the receptors to carry out a synapse between the skeletal muscle and a neuron, leading to a stop or weakening of muscle contraction. The decrease in the amounts of synapses cause the skeletal muscle to lose function, become weaker, and tire more easily.

Before I start with my topic, I feel that it is important to thank my instructors, Joey Battles and Katie Fulton, for such a great assignment. I truly enjoyed researching my topic of Guillain-Barré syndrome (GBS). Now that I have researched this disease I can now understand and sympathize with my dad, who developed GBS in 2005.

A historical perspective and classification of OBPP was first described by the Scottish obstetrician William Smellie in an article for midwives in 1764 [1] He documented the observation of resolution of bilateral upper extremity paralysis in a child with face presentation at birth. Danyau performed an autopsy of a newborn with brachial plexus palsy in 1851, providing the first anatomic description of this lesion.[2] but classic description of shoulder paralysis, internal rotation contracture and waiter’s tip deformity was given by Erb in 1874 as cited by Gilbert A et al. [3,4]. Duchenne and Balliere and Erb described cases of upper trunk nerve injury, attributing the findings to traction on the upper trunk, now called Erb’s palsy (or Duchenne-Erb’s palsy).[5]

After all three days of research, I had now gathered all my information and answered almost all my questions. From Myasthenia.org I figured out that the most common form of MG is a chronic autoimmune neuromuscular disorder. The symptoms vary but the main symptom is muscle weakness in the eyes, neck, and limbs. With severe cases of MG (such as a class 4 or 5 MG) the weakness in the mouth or respiratory may be more prominent. This muscle weakness is caused by blocked receptor sites. These receptor sites help involuntary muscles, when they are blocked it causes the weakness. Some cases of MG can have as much as 80% reduction of activeness in some receptor sites. Most symptoms are not immediately recognized as MG but the initial set off of