According to Medical-Surgical Nursing: 7th edition, Myasthenia Gravis (MG) is an autoimmune disease that can be considered as a chronic neuromuscular disorder (Lewis et al., 2007, p. 1555). MG is caused by an autoimmune process in which “antibodies attack acetylcholine (ACh) receptors, resulting in a decreased number of ACh receptor (AChR) sites at the neuromuscular junction” (p. 1555). Due to the neurotransmitter’s inability to connect the muscles and the nerves, it is difficult for the muscle to contract. This disease basically causes muscle fatigue and therefore a detrition of muscle strength over time. (John Hopkins Medicine, n.d.) In many respects, it is like a satellite unable to detect a signal when it is blocked by interfering radio waves.
The Yale School of Medicine’s online article concerning Myasthenia Gravis states that the term MG was first coined in 1672 by Thomas Willis. Simpson, in 1960, unveiled the mystery of MG when he theorized that it was caused by antibodies turning against the acetylcholine receptor (Yale School of Medicine, 2012). This was also proven by scientists Simpson and Nastuck observed so in 1959, who demonstrated that it was an autoimmune disease that had no connection to genetics (Conti-Fine, Milani and Kaminski, 2006).
Symptoms that occur when a person contracts Myasthenia Gravis often begin with the drooping of the eyelids. Clinical Reference Systems (2010) state that as the disease progresses, blurred vision and difficulty in maintaining a steady gaze begin to happen due to further weakness in eye muscles. Face paralysis is common, as well as slurred speech and difficulty of breathing, chewing, or swallowing due to weakness in the face and throat. This often leads to gagging, drooling, or...
... middle of paper ...
...s/myasthenia_gravis.html
Myasthenia Gravis. (n.d.). In John Hopkins Medicine. Retrieved February 20, 2012, from http://www.hopkinsmedicine.org/healthlibrary/conditions/adult/nervous_system_disorde rs/myasthenia_gravis_85,P07785/
NINDS Myasthenia Gravis Information Page. (2011, October 17). In National Institute of Neurological Disorders and Stroke. Retrieved February 20, 2012, from http://www.ninds.nih.gov/disorders/myasthenia_gravis/myasthenia_gravis.htm
Lewis, S., Heitkemper, M., Dirksen, S., O’Brien, P., & Bucher, L. (2007). Medical-surgical nursing: Assessment and management of clinical problems. (7th ed). Philadelphia, PA: Mosby Inc.
Yale School of Medicine (2011). Myasthenia Gravis. Retrieved November 19th, 2011, from Yale School of Medicine Web site: http://medicine.yale.edu/neurology/divisions/neuromuscular/mg.aspx
Physiological Basis of disease: DMD is the commonest and most serious form of the dystrophies. The gene responsible for dystrophin which, when absent, causes DMD. Amount of dystrophin correlates with the severity of the disease (i.e., the less dystrophin present, the more severe the phenotype). Since the gene is on the X chromosome, it primarily affects males, and females who are carriers have milder symptoms ( www.nlm.nih.gov/medlineplus/ency/article/000705.htm).
As motor neurons degenerate, this obviously means they can no longer send impulses to the muscle fibers that otherwise normally result in muscle movement. Early symptoms of ALS often include increasing muscle weakness, especially involving the arms and legs, speech, swallowing or breathing. When muscles no longer receive the messages from the motor neurons that they require to function, the muscles begin to atrophy (become smaller). Limbs begin to look thinner as muscle tissue atrophies (Choi, 1988).
The diagnosis for MG is often very difficult. Since there are many disorders that cause weakness, a number of tests may be used to determine a diagnosis of MG. In addition to a complete medical and neurological evaluation, a blood test for the abnormal antibodies can be completed to see if they are present. Three studies are used for the diagnosis of MG, anit-AchR antibody titers, the Tensilon test, and electromyography, including both the Jolly test and single fiber EMG. Used together, these three studies are almost 100% sensitive for Myasthenia Gravis.
Nonspeech signs associated with hypokinetic dysarthria may include characteristics dealing with the face, eyes, hands, arms, and trunk. The individual may have an expressionless look to their face as well as weakness with gestures in the hands, arms, and face that would normally match the person’s prosody when speaking. Overall, their social interaction with others can be emotionless. Eye blinking occurs less frequently than normal and their head gaze does not match where their eyes are looking. These patients swallow infrequently which leads to drooling. A tremor may be present in the jaw, lips, and tongue as well as limited movement during speech even though strength of these structures is often normal.
Fibromyalgia Syndrome (FMS) is a musculoskeletal illness (which causes chronic pain) and a chronic fatigue disorder. It can also change sleep patterns and cause the following: digestive disorders, chronic headaches, painful menstrual periods, temperature sensitivity, morning stiffness, numbness or tingling of extremities, and even cognitive memory problems. The name fibromyalgia comes from "fibro" in Latin meaning tissue, "my" in Greek meaning muscle, and "algia" (also Greek) meaning pain.(source 5)
James’s biopsy of his right gastrocnemius muscle would have shown a degeneration of the muscle or skeletal fibers due to the lack of dystrophyn. Another microscopic change that would be noticed is the accumulation of white blood cells. White blood cells have a very specific function which is to clear the damaged muscle fibers from the debris. Clearly, due to some of the muscle fibers being damaged other healthy fibers that have not been damaged appear denser. By having damaged muscle fibers, all the work rest upon the healthy fibers making them contract to the fullest due to the fact that the myosin and acting would have to overlap even more to make the muscle work.
Fibromyalgia is not a new disease that has just surfaced, it has been around for a long time, it just didn’t have a name and was not recognized for what it truly was. It was...
“Dystrophy,” originally coming from the Greek “dys,” which means “difficult” or “faulty, and “trophe,” meaning “nourishment” holds the interpretation “poor nutrition.” Today we know poor nutrition is not the cause of Muscular Dystrophy (“Myotonic Dystrophy”). Muscular Dystrophy is a genetic disorder that affects between 500-600 newborns each year in the US (Statistics on Muscular Dystrophy). In general, this disorder weakens your skeletal muscles, and eventually they degenerate. Muscular Dystrophy also has several specific types within the disorder, such as: Duchenne Muscular Dystrophy, Becker Muscular Dystrophy, and Myotonic Dystrophy. Each one has their own specific characteristics.
problems within the specific ion channels known to cause the disease. The goal of the
Body image has primarily been a problem for females. Recently, however, this view has opened up and has been seen in males. While women fixate on looking thin and slim, men’s obsessions are on the opposite spectrum, where guys want to be big, thick, and muscular. First known as "reverse anorexia", and now properly called muscle dysmorphia this obsessive compulsive disorder makes individuals believe that they are small and muscularly undeveloped and meanwhile they are moderately or highly muscular. This disorder is mostly seen in males and is rather unhealthy because it raises potential for self-esteem issues, steroid abuse, anti-social attitude, stress, over-meticulous diets and workout plans, and in worst case scenarios, suicide. In our society ideal body image for males has been put up to an impossible pedestal and the examples for the perfect physique are worsened by media causing this disorder to grow even further.
The first historical account of muscular dystrophy was identified by Sir Charles Bell in 1830. He wrote about a disease that caused weakness in boys that progressively got worse. In 1836 another scientist whose name is unknown reported about two brothers who developed muscle damage, generalized weakness. Also damaged muscle was replaced with fat and connective tissue. At the time the symptoms were thought to point to tuberculosis. During the 1850s reports of boys with progressive muscle weakness became more and more common. There were also reports of these boys losing the ability to walk and dying at an early age. In the next decade French neurologist Guillaume Duchenne gave and in depth account of 13 boys who had the most common ...
When a person begins to suffer from Guillain- Barre Syndrome their myelin sheath of their nervous system is being attacked and destroyed by the immune system (NINDS, 2011). The myelin sheath begins to lose its ability to transmit signals rapidly and affectively. Since signals are not getting transmitted to the brain fast enough, a person begins to notice fewer sensory responses from the rest of the body (NINDS, 2011). A person wouldn’t be able to tell right away or at all if an item they are touching is hot, cold, or causing pain. There also wouldn’t be good signal transmission from the brain to the rest of the body (NINDS, 2011). There would be signs of the muscles being unable to respond to the weakened or distraught signals they were receiving. Since the myelin sheath is responsible for transmitting the signals from a long distance, the upper and lower extremities would be the first to show signs of muscle dysfunction.
What causes Bell’s palsy is not clear, but some experts believe it is linked to the herpes simplex virus, that causes cold sores or Influenza. Many health problems can cause weakness or paralysis of the face. This is a form of cranial mononeuropathy VII, which is the 7th cranial facial nerve and the nerve controls the movement of the face. Bell’s palsy could also be linked to inflammation of the nerve in the area where it travels through the bones of the skull. And other such conditions as diabetes, and Lyme disease the symptoms for Bell’ palsy is as follows.
Guillain-Barré Syndrome (GBS) is an acute immune-mediated polyneuropathy that results in the rapid development of weakness in the muscles of the limbs and often also includes the muscles of the face, swallowing and respiration.1,2 Common symptoms associated with GBS include weakness, pain, tingling in the limbs and loss of deep tendon reflexes.1,2,3 The cause of GBS is still undergoing investigation, but it is believed to be the result of a preceding bacterial or viral infection. Currently, GBS is diagnosed via a spinal tap that examines cerebrospinal fluid for elevated levels of albumin and through electrophysiology studies which demonstrate decreased conduction velocities.3 There have been many proposed treatments for Guillain-Barré Syndrome
Multiple sclerosis (MS) is an acquired demyelinating disease of the central nervous system (CNS) that typically is diagnosed in the second or third decade of life. Normally, nerves are enclosed in myelin sheaths that help facilitate transmission of nerve impulses within the CNS and the peripheral nervous system throughout the body. In patients with MS, the myelin sheath is damaged and eventually degenerates, causing patches of scar tissue called plaques or lesions to occur anywhere randomly on the myelin sheath (Ruto, 2013). This results in impaired nerve conductivity, which interferes with message transmission between the brain and the other parts of the body. As a result, impulse transmission is altered, distorted, short-circuited, or completely absent. This interference in impulse transmission creates muscle weakness, muscle imbalance, and possibly muscle spasms with partial or complete paralysis. Multiple sclerosis also can result in visual impairment and alteration of cognitive abilities, as well as pain, numbness, or tingling sensations (Ruto, 2013).