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Guillaian-barre
Guillaian-barre
CHAPTER 46 MED SURG QUIZLET for 27. Guillain-Barre Syndrome
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Guillain- Barre Syndrome (GBS) is a rare, but very fatal auto- immune disease that specifically focuses on attacking the myelin sheath that surrounds the peripheral nerves in the human body. There are many different severities of this disease, but without treatment it can not only affect the entire nervous system but eventually shut down the rest of the body.
The myelin sheath is a fatty substance that surrounds the axons of the nerves and provides protection. It allows messages to be sent rapidly and accurately to the axons from long distances (Serono, 2010). The axons are the part of the nervous system that allows electrical transmission of signals throughout the brain and spinal cord. Without these electrical transmissions, the body would not be able to function properly (Serono, 2010).
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.
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Guillain-Barre Syndrome. (2011, August 1). Retrieved from https://www.medical-library.org/journals3a/guillain_barre_syndrome.htm
Mayo Clinic. (2011, May 28). Guillain- Barre Syndrome. Retrieved from http://www.mayoclinic.com/health/guillain-barre-syndrome/DS00413
MedPedia. (2012). Guillain-Barre Syndrome. Retrieved from http://wiki.medpedia.com/Guillain-Barre_Syndrome#Physical_Therapy
NINDS. (2011, July). Guillain- Barre Syndrome Fact Sheet. Retrieved from http://www.ninds.nih.gov/disorders/gbs/detail_gbs.htm
Serono, M. (2010, September 24). How does the Central Nervous System (CNS) Work?. Retrieved from http://www.epgpatientdirect.org/multiple-sclerosis/how-does-the-central-nervous-system-cns-work.cfm
Web MD. (2011, April 28). What Causes Guallain-Barre Syndrome? Retrieved from http://www.webmd.com/brain/tc/guillain-barre-syndrome-topic-overview
It was the beginning of February when my grandfather was going in to receive his second knee replacement. Being his second time, we were optimistic that the surgery would go well and that he would recover without any issues. My grandfather made it through surgery and accordingly, had to stay for observation. During this time everything appeared to be normal, and knowing that my grandfather hates to be in hospitals, wouldn’t have said otherwise. When he was finally discharged, we took him home and the next day he appeared to have a stroke. The left side of his face had drooped down and he began feeling numbness and tingling on both sides of his body. We immediately rushed him to the hospital and at first it was assumed it was a stroke, but as his illness progressed it was apparent it was not. The numbness soon led to the loss of muscle control beginning at his legs and rapidly spreading up. My grandfather was able to specifically describe what he was experiencing and the doctor was able to diagnose him with Guillain- Barré syndrome.
Pain behind the ear on the affected side of the face which may occur a day or two before the paralysis begins.
pathophysiology of the disease starts when the myelin sheath of both the spinal and cranial
Multiple sclerosis (MS) is a disease affecting the myelination of the central nervous system, leading to numerous issues regarding muscle strength, coordination, balance, sensation, vision, and even some cognitive defects. Unfortunately, the etiology of MS is not known, however, it is generally thought of and accepted as being an autoimmune disorder inside of the central nervous system (Rietberg, et al. 2004). According to a study (Noonan, et al. 2010) on the prevalence of MS, the disease affects more than 1 million people across the world, and approximately 85% of those that are affected will suffer from unpredictably occurring sessions of exacerbations and remissions. The report (Noonan, et al. 2010) found that the prevalence of MS was much higher in women than in men, and that it was also higher in non-Hispanic whites than in other racial or ethnic groups throughout the 3 regions of the United States that were studied.
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 (...
Lou Gehrig's disease is often referred to as Amyotrophic lateral sclerosis (ALS), this is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Motor neurons come from the brain to the spinal cord and from the spinal cord to the muscles throughout the entire body. The progressive degeneration of the motor neurons in ALS would eventually leads to their death. When the motor neurons die, the ability of the brain to initiate and control muscle movement is also lost. With voluntary muscle action progressively affected, for this reason patients in the later stages of the disease may become totally paralyzed (Choi, 1988).
Well have you ever wonder what Multiple Sclerosis? Today i'm going to explain to what MS(Multiple Sclerosis) is so I hope that you enjoy.
Multiple sclerosis (MS) is generally thought to be an autoimmune disease that attacks the myelin sheaths, or oligodendrocytes that cover nerve axons in the central nervous system (PubMed Health 2013). This immune response causes inflammation, which triggers immune cells to destroy axons “along any area of the brain, optic nerve, and spinal cord” (PubMed Health 2013). When the myelin sheath “is damaged, nerve signals slow down or stop” thus hindering the propagation of action potentials and limiting function (PubMed Health 2013).
...dison, N. (2014, March 14). What is the Difference Between Schizophrenia and Multiple Personality Disorder? Retrieved from Wisegeek.com: http://www.wisegeek.org/what-is-the-difference-between-schizophrenia-and-multiple-personality-disorder.htm
The earliest symptoms of ALS are weakness of the muscles, which is to be expected. These types of symptoms can involve having trouble swallowing, cramping, or stiffness of certain muscles. As the disease progresses, patients lose the ability to control all voluntary movements. Generally, sensory nerves and the autonomic nervous system are unaffected, meaning that individuals with ALS can hear, see, touch, smell, and taste properly. The types of muscles you are able to control by the early symptoms, all depends on which motor neurons are damaged first. The most common motor neurons that get damaged early on are the ones called “limb onset,” which have to do with the arms and legs. As expected, people with “limb onset” experience trouble when walking and running, such as stumbling, tripping, or dragging of the foot. Other types of “onsets” that ALS patients might experience, is “bulbar onset” and “respiratory onset.” Bulbar onset ALS patients have a difficulty time speak...
(Marieb, 2016). Myelin is the protective coat surrounding and insulating the nerve fibers of CNS. Myelin is fatty tissue substance that if attacked by immune cells causing a short-circuits in the current so that the successive gaps are excited more and more slowly, and eventually impulse conduction ceases which resulted in various forms of symptoms (Marieb, 2016). The degradation could either be “by inflammation, stroke, immune disorder, metabolic disorders, or nutritional deficiencies” (Slomski, 2005). The target that immune cells are sensitized to attack remains
Tay-sachs disease is perhaps a very dramatic disease because it strikes most keenly at small children and babies. The disease is very rare and fatal. Tay-sachs is a genetic disorder in which harmful amounts of fatty lipids, known as ganglioside GM2, is built up in the nerve cells in the brain. Infants who with Tay-sachs disease, who are not carriers, appear to develop normally for the first few months since their birth, but as the nerve cells become swollen with the fatty material, a severe decline of mental and physical abilities occurs. The child then becomes deaf, blind, and unable to swallow.
This reduces the amount of current that would otherwise leak out of the axon and increases the distance that the current can flow passively. Myelination, aka axon insulation, increases action potential conduction up to 150m/s compared to 0.5-10m/s conduction velocities of unmyelinated axons! Speedy delivery of current information along axons is also due to the nodes of Ranvier. Nodes of Ranvier are gaps between insulated portions of the axon. The gaps create a place where the current can flow out of the axon so an action potential can be generated.
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.
The brain consists of both neurons and glia cells. The neurons, which are cells housed in a cell body called a Soma, have branches which extend from them, referred to as dendrites. From these dendrites extend axons which send and receive impulses, ending at junction points called synapses. It is at these synapse points that the transfer of information takes place.