Myasthenia Gravis : An Autoimmune Neuromuscular Disorder

A. In 1994, Karen was diagnosed with Myasthenia Gravis (MG), which is a rare neuromuscular disease. It was understood that this is what she had been

Myasthenia Gravis (MG) is a chronic autoimmune disorder of the neuromuscular system part of the body. Chronic means persisting for a long time or constantly recurring. Autoimmune disorder is the confusion of the body’s immune system. The immune system form antibodies that mistakenly identify healthy tissue as foreign and then, the antibodies will attack and/or destroy healthy body tissue. Neuromuscular is the nervous system relationship with the muscles bring about body movement.

The study enrolled 306 recent stroke victims with dysphagia, as defined by the WHO standards. The participants were split into groups of 102 that was randomly assigned by a computer generated program to remove bias. The three groups consisted of “usual care”, “low intensity care”, and “high intensity care”. Before carrying out therapy, all participants were given a videofluoroscopy as baseline data. One baseline data was carried out, the different groups started treatment. The low/high intensity care consisted of swallowing compensation strategies, (upright position while eating), appropriate dietary modifications (thickening of liquid food), and the teaching of safe swallowing techniques ( reduced rate of eating). The two experimental groups only differed by the amount of sessions per week. The low intensity group was seen 3 times a week for 1 month, and the high intensity group was seen every working day for 1 month.

Symptoms that arise due to Myasthenia gravis include common conditions such as drooping eyelids, muscle fatigue and loss of fine motor control that can be attributed to many other conditions as well. This can make diagnostics very tricky but thanks to the great understanding obtained through research into the disease, the diagnosis of Myasthenia gravis is fairly straightforward and there are a few techniques used as accepted tests.

Lambert-Eaton myasthenic syndrome, also known as Eaton Lambert syndrome, is an autoimmune disease that is characterized by the onset of severe muscle weakness. The muscle weakness involved with Lambert-Eaton myasthenic syndrome (LEMS) typically occurs in the pelvis and thigh muscles. Approximately 60 percent of LEMS cases are associated with a small cell lung cancer (SCLC), and the onset of LEMS symptoms often precedes the detection of the cancer (Gozzard). Patients who have LEMS that also have cancer tend to have a history of smoking and are usually older adults. LEMS occurs often in men with tumors in their chests, especially lung cancer. Individuals without cancer can develop LEMS at any age. However, LEMS is rarely seen in children and this disease is not hereditary. This disease is also more common in men than in women and the progression depends on whether it occurs with cancer.

Because Myasthenia Gravis is such a rare disease, it makes it difficult for medical professionals to diagnose it, often leading to misdiagnoses. The first reported case of the what is now recognized as Myasthenia Gravis was documented in 1664 of Native American Chief Opechancanough whose “mystery illness” caused “the excessive fatigue he encountered to wreck his constitution…his sinews lost their tone and elasticity; and his eyelids were so heavy that he could not see unless they were lifted up by his attendants… he was unable to walk…” It is believed that the mystery illness afflicting the chief was most likely Myasthenia Gravis due to the hallmark symptoms of fatigue, bulbar & ocular weakness as well as overall muscular weakness in the arms and legs. Because the facial muscles are also affected, other symptoms of Myasthenia Gravis include muffled speech, difficulty swallowing & chewing, and diplopia (double vision). In approximately 85% of MG patients, the disease becomes generalized and within 3 years, the limbs, axial muscular groups like the neck muscles, as

The decrease in the amount of AChRs is believed to be due to multiple mechanisms. Anti-AchR antibodies bind to and block target receptors, increase the turnover of receptors, and damage the postsynaptic membrane by fixing complement. Autoantibodies against the AChR are present approximately 80% of patients with MG. However, over 40% of the patients without antibodies to AChR will have antibodies directed against the muscle-specific receptor tyrosine kinase (MuSK). The MuSK protein is a transmembrane component at the postsynaptic neuromuscular junction. The MuSK complex mediates the clustering of AchR during NMJ formation

Myasthenia gravis (MG) is considered to be a very rare disorder. It is an autoimmune neuromuscular junction disease which in most cases occurs as a painless, massively fatigable weakness; targeting certain muscle groups. Some of the initial presentations of myasthenia gravis include the ocular weakness with binocular diplopia consecutively, along with asymmetric ptosis. Limb weakness is rare initially. Therefore, patients who experience ocular weakness as an initial symptom, usually do not develop the limb weakness until approximately three years later. Therefore, a primary care doctor must be strictly observant so as to find out the presence of myasthenia gravis. When the T cells-dependent immunologic react or attack the endplate area of the

Myasthenia Gravis is an autoimmune disease of the neuromuscular junction which usually causes muscle weakness and other problems. Some of the people who have Myasthenia Gravis experience respiratory failures. It’s very crucial that these patients stay away from interventions that might worsen the disease process. In 2014 a 62 year old woman with a history of metastatic thymic carcinoma and myasthenia gravis came to the emergency room in Houston, Texas. For two days this lady had been experiencing weakness, difficulty swallowing, and shortness of breath. They admitted her into the intensive care unit because she had the symptoms of a myasthenia crisis. That evening they ran a test and there was a substantial decrease in the patient’s vital capacity. The patient wouldn’t agree to be intubated or ventilated. On the third day in the ICU the patient was granted a trial of non-invasive ventilation, but this did not improve her condition. So finally she agreed to be intubated

With the logopedic treatment alone dysphagia had not decreased and the patient remained on a feeding tube (Baijens et al, 2008). The NMES treatment included two positions for the patient to be in. Position A included two sets of electrodes with an electrical current up to 10.0 mA, located on each side of the midline, above and beneath the lesser horns of the hyoid bone, on the myohyoid muscles and on the thyroid muscles (Baijens et al, 2008). Position B included one set of electrodes with an electrical current up to 17.5 mA, located on each side of the mouth on the orbicularis oris muscle and the masseter muscles (Baijens et al, 2008). The patient was offered various food consistencies using swallowing maneuvers to help with safe swallowing. A SLP did clinical assessments before and after treatment using functional oral intake scale for dysphagia (Baijens et al, 2008). After therapy the scale showed signs of improved feeding ability in the participant. The participant changed from a PEG tube feeding to an oral diet with special

LEMS can be either an autoimmune or a paraneoplastic condition. Antibodies are directed against the presynaptic P/Q voltage gated calcium channels (VGCC), resulting in reduced release from of acetylcholine.

Finding the best treatment for children with swallowing disorders is a problem many Speech-Language Pathologists are challenged with. Knowing the etiology is of the utmost importance when determining the appropriate treatment for the disorder. This articles emphasizes the significance of finding the etiology of the disorder. To find the etiology, a battery of test

John Stillman, a thirty-two year old gymnastics instructor, was presented to the clinic with complaints of muscle weakness in the face that comes and goes. Symptoms have progressed over the past two months to include tired jaw, difficulty swallowing, diplopia in the evening, increased weakness in his limbs and shortness of breath. Physically visible, John has mild ptosis in both eyelids and his smile is a bit off. Patient John Stillman portrays symptoms of Myasthenia Gravis (MG) meaning grave muscular weakness. According to Myasthenia Gravis Foundation of America, the most common form of MG is chronic autoimmune neuromuscular disorder, which can be seen by loss of strength in the voluntary muscle groups (2015). Much research has been done for Myasthenia Gravis, but there is still a lot of unknown information, such as a cure. In this study, one will learn what Myasthenia Gravis is, how it is tested, possible complications, and how it is treated.

Anderson Dysphagia Inventory (MDADI) as it is a valid and reliable survey designed specifically for evaluating the impact of dysphagia on QOL in patients who have undergone treatment for head and neck cancer. Patients were not randomized to the two treatment groups. Patients who were included in the study before the MDADI was available (12) were placed in the post-treatment therapy group. The MDAID consists of four QOL domains: global, emotional, functional, and physical. For the two treatment groups, mean scores for each domain as well as an overall swallowing QOL score using an average of the four domains was

“Achalasia comes from the Greek word khalasiswhich means “not relaxing” (Pandolfino and Gawron, 2015).Indications of achalasia include the “absence of oesophageal peristalsis and the incomplete relaxation of the Lower Esophageal Sphincter (LES) during which swallowing is difficult”(Steffens, Oumer, and Roberts, 2013). According to Izbicki, et al (2009), patients exhibit vomiting and weight loss as the disease progresses as LES does not relax with swallowing but carries on squeezing the end of the ooesophagus. A barrier is formed which stops the solids and the liquids from going to the stomach thereby accumulating volumes of such intake and eventually dilating the oesophagus further.The symptomatic result of the disorder is dysphagia which can progress to other symptoms, such