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Quiz on myasthenia gravis
Kennedy myasthenia gravis
Quiz on myasthenia gravis
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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 …show more content…
Normally when electrical signals or impulses travel down a motor nerve, the nerve endings release an acetylcholine. Acetylcholine activates the muscle and causes a muscle contraction. In myasthenia gravis, antibodies destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle from contracting. However, antibodies to other proteins, such as MuSK (Muscle-Specific Kinase) protein, can also lead to impaired transmission at the neuromuscular junction. Myasthenia gravis affects both men and women and occurs across all racial and ethnic groups. Commonly affects young adult women under the age 40 and older men over the age of 60. This disease is not inherited nor is it
In the beginning phases of muscle contraction, a “cocked” motor neuron in the spinal cord is activated to form a neuromuscular junction with each muscle fiber when it begins branching out to each cell. An action potential is passed down the nerve, releasing calcium, which simultaneously stimulates the release of acetylcholine onto the sarcolemma. As long as calcium and ATP are present, the contraction will continue. Acetylcholine then initiates the resting potential’s change under the motor end plate, stimulates the action potential, and passes along both directions on the surface of the muscle fiber. Sodium ions rush into the cell through the open channels to depolarize the sarcolemma. The depolarization spreads. The potassium channels open while the sodium channels close off, which repolarizes the entire cell. The action potential is dispersed throughout the cell through the transverse tubule, causing the sarcoplasmic reticulum to release
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.
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).
Flaccid dysarthria results from damage to the lower motor neurons (LMN) or the peripheral nervous system (Hageman, 1997). The characteristics of flaccid dysarthria generally reflect damage to cranial nerves with motor speech functions (e.g., cranial nerves IX, X, XI and XII) (Seikel, King & Drumright, 2010). Lower motor neurons connect the central nervous system to the muscle fibers; from the brainstem to the cranial nerves with motor function, or from the anterior horns of grey matter to the spinal nerves (Murdoch, 1998). If there are lesions to spinal nerves and the cranial nerves with motor speech functions, it is indicative of a lower motor neuron lesion and flaccid dysarthria. Damage to lower motor neurons that supply the speech muscles is also known as bulbar palsy (Pena-Brooks & Hedge, 2007). Potential etiologies of flaccid dysarthria include spinal cord injury, cerebrovascular accidents, tumors or traumatic brain injury (Pena-Brooks & Hedge, 2007). Possible congenital etiologies of flaccid dysarthria include Moebius syndrome and cerebral palsy. Flaccid dysarthria can also arise from infections such as polio, herpes zoster, and secondary infections to AIDS (Pena-Brooks & Hedge, 2007). Additionally, demyelinating diseases such as Guilian-Barre syndrome and myotonic muscular dystrophy can also lead to flaccid dysarthria (Pena-Brookes & Hedge, 2007). The lower motor neuron lesion results in loss of voluntary muscle control, and an inability to maintain muscle tone. Fasciculations, or twitching movements, may occur if the cell body is involved in the lesion (Seikel et. al., 2010). The primary speech characteristics of flaccid dysarthria include imprecise consonant production, hypernasal resonance, breathiness, and harsh voice (...
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).
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)
Muscular dystrophy (MD) is a genetic disorder that weakens skeletal muscles, the muscles that enable the human body to move. People with muscular dystrophy have missing or incorrect information in their genes, which prevents them from making the proteins they need for healthy muscles. Due to fact that muscular dystrophy is genetic, it is not contagious or contractible from another person; a person must be born with the problem.
Myotonic dystrophy, type 1, is a genetic disorder which is linked to chromosome number 19 in humans. The dystrophia myotonica protein kinase gene is located on the q arm of the chromosome at the locus of 13.32. It is an autosomal dominant disorder, which means that the individuals that are affected by this disorder and contain at least one dominant allele for the dystrophia myotonica protein kinase gene. The disorder is caused by a series of repeats of a trinucleotide region that is expanded beyond the normal levels (Musova et al., 2009). The trinucleotide region is a series of repeats of CTG in the untranslated region of the dystrophia myotonica protein kinase gene. The severity of the disorder is associated with the number of repeats the individual has within the gene. Normal individuals tend to have between 5 and 37 repeats while an individual with a very mild myotonic dystrophy may have 50 to 150 repeats, and if the disorder is discovered at the time of birth the individual will have over 2,000 repeats of the trinucleotide region (Musova et al., 2009). Myotonic dystrophy, type 1, affects multiple organ systems of the body and is relatively slow to progress. Myotonic dystrophy, type 1, is categorized by alterations of the beating pattern of the heart, faulty dystrophin proteins, clouding of the lens of the eye, decreased functionality of the gonads, balding, and myotonia (Musova et al., 2009). Myotonia is described as the slow relaxation of any muscle type, which will cause the individual to use extended effort to simply relax the muscles after they have been contracted. Muscular dystrophy causes an individual to experience muscular deg...
Muscular Dystrophy is a genetic disorder in which your muscles drastically weaken over time. Muscles are replaced with “connective tissue,” which is more of a fatty tissue than a muscular one. The connective tissue is the tissue that is commonly found in scars, and that same tissue is incapable of movement. Although Muscular Dystrophy affects muscles in general, other types affect certain groups of muscles, and happen at different periods throughout a lifetime. For example one of the most common types, Duchenne Muscular Dystrophy, targets muscles in the upper thigh and pelvis. The disease is displayed throughout early childhood, usually between ages four and seven. This genetic disorder occurs only in boys. People have difficulty sitting up or standing and lose their ability to walk in their early teens. Sadly most people die by the age of twenty. A second common type, Becker’s Muscular Dystrophy affects the same muscles as Duchenne, but first appears in teenage years. Most people with Becker’s only live into their forties (Fallon 1824-1825).
The human genome is a remarkable system composed of over 3 billion DNA base pairs that encode for the characteristics that makes people distinctly human and unique themselves. Without the genome’s nearly flawless ability to self-replicate the human species would cease to exist. As incredible as this replication methodology is, it is not without its faults. Genetic mutations, though rare and typically harmless, can strike at any time and in various ways. Still, when they do cause harm the effects can be profound and impossible to ignore. Hutchinson-Gilford Progeria Syndrome (HGPS) is an instance where the mutation of just one nucleotide has devastating results. The Mayo Clinic defines progeria as a progressive genetic disorder that causes children to age rapidly, beginning in their first two years of life. This study defines the disease of progeria by outlining symptoms and identifying causes that lead to its diagnosis. In addition, treatment methods and extensive research that give those affected by the disease hope for a brighter future are highlighted.
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 ...
Amyotrophic lateral sclerosis, or ALS, is a degenerative disease affecting the human nervous system. It is a deadly disease that cripples and kills its victims due to a breakdown in the body’s motor neurons. Motor neurons are nerve cells in the brainstem and spinal cord that control muscle contractions. In ALS, these neurons deteriorate to a point that all movement, including breathing, halts. Muscle weakness first develops in the muscles of body parts distant from the brain, such as the hands, and subsequently spreads through other muscle groups closer to the brain. Such early symptoms as this, however, can hardly be noticed.
With motor neurone disease it attacks the nerves, in the brain and spinal cord. This means messages gradually stop reaching muscles, which leads to weakness and wasting. In the case study the
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.
The first disease being discussed, Bell’s Palsy, is a disorder resulting in temporary facial paralysis due to damage to the facial nerves. It is the single most common form of facial paralysis; it usually occurs on one side of the face only. Symptoms start up quite suddenly and peak within 48 hours (NINDS, 2011). However, it is important to remember that symptoms vary person to person; some might feel mild weakness while others can experience total paralysis. The most common symptoms are weakness, paralysis, twitching, drooping of the corner of the eyelid or mouth, drooling, impairment of taste, etc and can sometimes cause facial distortion. Actually, viral meningitis or herpes simplex could cause this disease when the facial nerve swells in reaction the infection being carried (NINDS, 2011).