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...
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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
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.
Impairment and sometimes loss of motor control of the body and its extremities is one of the many effects of this disorder. Patients may complain of headaches, neck pain, coughing, sneezing, dizziness, vertigo, disequilibrium, muscle weakness, balance problems, and loss of fine motor control (1). The senses (hearing, sight, smell etc.) may also be affected in deleterious ways. On can have blurred vision, decreased sensation of limbs, unable to locate them without looking, decreased sense of taste, ringing of the ears etc. (2).
Myasthenia gravis (MG) is a chronic state that causes muscles to tire and weaken easily. The meaning of the term Myasthenia Gravis is broken up, My means Muscle, asthenia means lack of strength and Gravis means serious. In an autoimmune disorder the immune system attacks parts of the body. The part of the body that is attacked by the circulation of antibodies, is the muscular system, and in certain receptors for acetylcholine on muscle cells at the neuromuscular junctions.
Spinal Muscular Atrophy, also known as “SMA” is a genetic and also a motor neuron disease that affects the area of the nervous system that controls your voluntary muscle movements such as walking, crawling, and swallowing. When someone acquires this condition their muscles start to shrink as a cause to the muscles not receiving signals from the nerve cells in the spine that control function. Spinal Muscular Atrophy is a rare but serious condition.
Based on the apparent symptoms of the elderly patient consisting of muscle weakness and a drooping of the eyelids, it appears that the cause of illness is myasthenia gravis, a condition that weakens the voluntary muscles of the body. The cause of this eyelid drooping, or muscle paralysis in general, is due to a misstep in the flow from the nerve fiber to the muscle fiber. It is known that an action potential in the muscle fiber is required for muscle contraction. However, if the release acetylcholine is blocked, or the number of acetylcholine receptors is reduced, it causes a chain of events that prevent muscle contraction. This prevention of the binding of acetylcholine to the receptor prevents
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.
Myasthenia Gravis is a chronic autoimmune disorder that weakens the muscles. The name MG comes from the Latin words meaning grave muscle weakness. In 1672, Thomas Willis was the first to describe a patient with myasthenia gravis. There were periodic case descriptions over the years in 1900 regarding this disease. The disease remained a mystery, until 1960 when Simpson suggested that myasthenia gravis was caused by antibodies against the acetylcholine (ACh) receptor. Patrick and Lindstorm both proved that myasthenia gravis is autoimmune in origin by testing rabbits that were immunized with Torpedo ACh receptors became myasthenic. Today, myasthenia gravis is one the most thoroughly understood neurological disorders. This has lead to an overall understanding of the disease such as the cause associated, risk factors, complications, incidences, organ systems affected, signs and symptoms, diagnosis, and treatments, which enormously improve the length and quality of life for these individuals.
Because symptoms are wide - ranged and studies for treatment of FMS did not begin until the 1980's, it is one of the most popularly misdiagnosed conditions in the medical world. The main symptoms are widespread pain and fatigue as well as tender points on the body. The muscular pain often may feel like a pulled muscle and may burn or twitch. (Source 3)
GBS is also known as acute inflammatory demylinating polyneuropathy and Landry's ascending paralysis after Jean B. O. Landry, a French physician who described a disorder that "paralyzed the legs, arms, neck, and breathing muscles of the chest." (4) (1) GBS was named after French physicians Georges Guillain and Jean Alexander Barre who, along with fellow physician Andre Stohl, described the differences of the spinal fluid of those who suffered f...
Guillain-Barre Syndrome is an autoimmune disorder where the immune system attacks the nervous system, especially that of the Peripheral Nervous System, PNS. The PNS connects to the Central Nervous System, CNS, which allows the limbs and organs to react/function. Tissues and organs affected are the peripheral nerves and muscle movements. GBS can range from severe to minor,...
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 ...
Myasthenia gravis is a chronic auto-immune neuromuscular disease, which causes weakness in the skeletal muscles. These muscles are responsible for breathing and moving certain parts of the body. The number one sign of myasthenia gravis is muscle weakness that worsens after periods of activity and improves after periods of rest. The eyes are usually affected first with this disease. MG tends to attack muscle groups used for voluntary movement, meaning they are muscles that you have control of. Certain muscles such as those that control facial expression, chewing, talking, and swallowing are often involved with this disease. Because weakness is a common symptom of many other disorders, the diagnosis of myasthenia gravis is often missed or delayed
Myasthenia Gravis (MG) is an autoimmune disorder affected the neuromuscular junction and the process of neuromuscular transmission. MG is a disease that reflects an autoimmune response against acetylcholine (ACh) receptors at the postsynaptic membrane at the motor endplate (Duffy, 99). Because there are a reduced number of operative receptors, the muscle responsiveness to the Ach that sparks muscle contraction is reduced. The repercussion for this is diminishing muscle contractions with repetition of use. With rest and time for nerves to reload the Ach supply, strength of the muscles may improve.
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.
It usually appears after spinal shock has subsided and is part of an upper motor neuron (UMN) syndrome. Other symptoms related to spasticity are muscle spasms, an abnormal increase in muscle tone, overactive stretch reflex, and clonus. Multiple causes can contribute to an increase in spasticity including but not limited to: changes in positions, the temperature of the environment, tightness of clothing, urinary/digestive complications, emotional stress, pressure ulcers, or a quick passive stretch to the spastic muscle. The severity of spasticity varies, and SCIs who have been diagnosed with spasticity reports it as being problematic; however, if those with mild to moderate involvement are taught how to control the onset of spasticity or spasms at specific times, this could be used to the individual’s advantage in helping with functional tasks such as transfers. On the other hand, if the spasticity is severe it can cause major problems with functional tasks. Treatment of spasticity typically includes slow-controlled stretching exercises, modalities, and medications. Common medications are muscle relaxants and spasmolytic agents such as baclofen, diazepam, tizanidine, and dantrolene sodium. Botulinum neurotoxin (botox) may also be given intramuscularly to manage focal spasticity. Surgical intervention may be required if all other treatments have failed. Surgical procedures that may be