Guillan Barre Syndrome Essay

Topics: 32082989 Guillan Barre Syndrome

Specifications: 3 pages, 4 sources, APA style

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Description: Preferred language style: English (U.S.)
As per the Instructor
I-The Introduction should be written in a chronological format. How the disease was discovered and how and when it was published. At the end of the introduction, mention latest article about the topic.
Body of paper: Review of your articles
II- Discuss methods of investigation employed by the researcher and how the topic got evolved and how things are being gradually understood now.
III-Personal Approach to subject
-new drugs
-new experimental approach or new suggestion for research. That will be incorporated in the conclusion.

Guillain-Barre Syndrome (GBS) or ‘acute idiopathic polyneuritis’ is a condition in which the individual immune system begins to attack the own tissues (rapidly progressing autoimmune disorder), especially the peripheral nerve tissues, usually after a bacterial or viral infection (usually a digestive tract or a respiratory tract infection).  Such an infection is observed in about 60 to 70 % of all cases.  The individual develops tiredness, muscle weakness, abnormal sensations in the lower limbs (and upper limbs), paralysis, respiratory difficulties, etc (NINDS, 2007).  In rare cases, portions of the brain and the spinal nerves may be involved with the disease (Griffin, 2000, pp. 2192 and Mayo Clinic, 2006).  The condition may also occur after surgery or immunization (Cull, 1996, pp. 1106).  The can occur in both males and males and in all age and cultural groups.  It is very rare in occurrence (one in every 100, 000 individuals in the US, annually) (Mayo Clinic, 2006).  Once the condition begins, it tends to progress over the next few weeks or days (NINDS, 2007).  In the less developed nations (such as the US and Europe), acute versions of the disease occur more frequently (Griffin, 2000, pp. 2192).

In the year 1848, Graves found that paralysis occurred due to a defect in the nervous system.  Landry de Thezillat described ascending paralysis in the year 1859.  This description was following certain case studies that Landry performed on about 5 patients suffering from GBS.  One of these patients had died later affected with a serious respiratory condition.  Landry even predicted the early death of one of his patients who suffered from hysteria during the early stages of the disease.  Later, Landry found that the patient suffered from the condition in which paralysis occurred following an infection.  This paralysis usually occurred due to demyelination of the nerves.  The term GBS was first utilized in 1927 by Claudian and Dragonescu.  The term was derived from the famous French neurologists Gullain and Barre from Paris.  They were serving as doctors in the French army during the World war One, and observed that some soldiers had suffered from progressive muscle paralysis that occurred following infection.  Strohl along with Gullain and Barre published a paper in the year 1916 describing the disease (GBS-UK, 2005).

Earlier the cause of GBS was not understood clearly.  However, recent studies begin to show that the disease is caused due to a defect in the functioning of the immune system.  This may be triggered by a bacterial or a viral infection.  Scientists have even begun to observe that the disease is not contagious and is not transmitted from one individual to another.  Initially, the manner in which the autoantibodies were formed was clearly not understood.  These antibodies begin to attack the myelin sheath that forms a protective insulation on the nerves, resulting in its degeneration.  The nerve signals usually jump during the transmission of the nerve signals from certain points on the nerve fibers known ‘node of Ranvier’.  This ensures that the nerve signals are transmitted in a speedy manner.  However, if the myelin sheath is destroyed, the nerve signals cannot be transmitted, and the muscles are unable to function normally as per the directions of the brain.  Besides, those nerve signals that carry sensory information to the brain 9senory nerves) may also undergo demyelination resulting in the development of parasethesia, stinging sensation, etc (NINDS, 2007).  GBS can occur following a number of infections with a variety of bacteria and viruses such as C. Jejuni infection (the most severe of them all), Herpes infection, infectious mononucleosis, Epstein Bar Virus infection, Cytomegalovirus infection, and Myoplasma infection.  The rates of GBS developing in indiviauls suffering from a bacterial infection are two in every ten thousand (Tam, 2006).

GBS has to be managed in a comprehensive manner to ensure that the symptoms are controlled and do not affect the normal functioning of the individual.  As the signs and symptoms of the disorder are varied and depends on several other factors, a thorough evaluation of the patient needs to be conducted.  The history, symptoms, signs, physiological nerve conduction tests, lumbar puncture, blood tests, electromyography, etc, play a very important role in the diagnosis of GBS.  A record should be made of the patient’s muscle weakness and the sensory defects.  EMG (electromyography) is needed to determine the electrical activity of the muscles and nerve stimulation tests are required to study the speed at which the nerves conduct electrical signals (Mayo Clinic, 2006).  In GBS, the rate at which these signals are transmitted is usually reduced.  The level of proteins in the CSF is usually raised (which is suggested by lumbar puncture) (NINDS, 2007).  At present there is no specific treatment available to treat GBS.  Usually treatment is provided to help reduce the symptoms of GBS, and also prevent the development of complications.  The lung function, swallowing functions, nerve activity, etc, have to be continuously monitored to ensure through appropriate tests.  Nowadays, a lot of research is being conducted in the use of Corticosteroid, immunoglobulins and Plasmapheresis in the treatment of GBS.  Besides, rehabilitation therapy also seems to be effective in the long-term management of the patient.  Corticosteroid therapy (helps to reduce the symptoms of the disease) may not seem to manage the condition effectively alone, and this treatment has to be combined with other treatment measures (Griffin, 2000, pp. 2193 & NINDS, 2007).  Plasmapheresis (or plasma exchange) is usually performed along with administration of immunoglobulins in order to improve the response to treatment.  The blood may consist of several immune-mediated substances that may bring about the symptoms of GBS, and through plasma therapy, these substances are effectively removed.  Besides, immunoglobulins are administered to ensure that the body has an effective mechanism to fight bacteria and viruses.  These immunoglobulins help to fight any antibodies that could initiate the symptoms of GBS (Mayo, 2006 & NINDS, 2007).  Besides, research also needs to be conducted in the field of physical therapy and hydrotherapy, as these seem to be promising to rehabilitate the patient following an attack of GBS.  Studies have shown that these therapies may seem to be effective in reducing the severity of several permanent disabilities such as muscle weakness and respiratory difficulties (Griffin, 2000, pp. 2193).  Studies have shown that when Plasmapheresis is conducted, it takes about 3 months for an individual to recover from an attack for GBS, and about 6 months in case it is not conducted.  Recovery may occur in about eight out of ten patients (Cull, 1996, pp. 1106).  The recover rate significantly varies, and about one in every ten individuals meets with fatal outcome (Cull, 1996, pp. 1106).  Studies have shown that using Plasmapheresis along with immunoglobulins administration can treat recurrences.

References:

 Cull, R. E., and Will, R. G. (1996). Diseases of the Nervous System, In. Edwards, C. R. A., Bouchier, I. A. D., & Haslett, C. (Ed), Davidson’s Principles and Practice of Medicine, (17th Ed), Edinburgh: Churchill Livingstone.

GBS Support Group UK (2005), The History of GBS and CIDP, Retrieved on August 1, 2007, from GBS-UK Web site: http://www.gbs.org.uk/history.html

Griffin, J. W. (2000). Immune-mediated Neuropathies, Goldman, L. and Bennett. J. C. (Ed) Cecil Textbook of Medicine, (21st ed, Vol. 2), Philadelphia: W. B. Saunders.

Mayo Clinic staff (2006). Guillain-Barre Syndrome. Retrieved on August 1, 2007, from Mayo Clinic Web site: http://www.mayoclinic.com/health/guillain-barre-syndrome/DS00413/DSECTION=1

National Institute of Neurological Disorders and Stroke (2007). Guillain-Barre Syndrome Fact Sheet. Retrieved on August 1, 2007, from NINDS Web site: http://www.ninds.nih.gov/disorders/gbs/detail_gbs.htm

National Institute of Neurological Disorders and Stroke (2007). NINDS Miller Fisher Syndrome Information Page.  Retrieved on August 1, 2007, from NINDS Web site: http://www.ninds.nih.gov/disorders/miller_fisher/miller_fisher.htm

Tam, C. C., Rodrigues, L. C., Petersen, I. et al (2006). ”Incidence of Guillain-Barre syndrome among patients with Campylobacter infection: a general practice research database study.” J Infect Dis, 194(1), 95-97. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=16741887