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         Acute Idiopathic Polyneuritis:     more detail
  1. GBS, Guillain-Barre syndrome (acute idiopathic polyneuritis): An overview for the layperson by Joel S Steinberg, 1983
  2. GBS, Guillain-Barré syndrome: Acute idiopathic polyneuritis and chronic inflammatory polyneuropathy : an overview for the layperson by Joel S Steinberg, 1995

101. C:\FILES\ARTICLES\ml135may94.htm
Patients sent to other hospitals for less acute care or rehabilitation were notreviewed. The inflammatory lesion in idiopathic polyneuritis. Medicine.
http://www.brown.edu/Departments/Clinical_Neurosciences/articles/ml13594.html
Guillain-Barre Syndrome:
A 5-year Rhode Island Hospital Experience
May Louie, MD, James M. Gilchrist, MD, Craig Woodard, MD, PhD GBS is the result of a cell-mediated immunologic attack upon Schwann cells and nerve myelin.[3] The trigger is unknown but has been postulated to be related to recent infection in a majority of patients[4,5] Macrophages invade the endoneural structures, disrupting Schwann cells and phagocytizing myelin segmentally and near the Nodes of Ranvier.[3] Proximal nerves are affected
preferentially, such as ventral nerve roots, nerve trunks and plexuses, though more distal peripheral nerves and autonomic ganglia also are affected.[3] The axon is not involved initially except for a rare axonal variant [6] but can be destroyed in severe forms of the disease. Schwann cells survive and retain the ability to divide and form new myelin. Recovery depends upon remyelination, which can begin within 2 weeks of onset, and axonal regeneration, which continues at a much slower rate and can take many months to complete. Despite the reversible nature of the neurologic deficits in GBS, intervention through plasmapheresis clearly can shorten hospital stay, improve time to independent walking and decrease time on mechanical ventilation.[7] The most widely held indication for plasmapheresis in GBS is inability to walk 5 meters unassisted, which encompasses the majority of GBS patients.[7] Recently, a Dutch study has indicated intravenous human immune globulin may be as beneficial as plasmapheresis.[8]

102. EMedicine - Guillain-Barré Syndrome Article By Michael A
Synonyms and related keywords nerve disorders, myelin, acute idiopathicpolyneuritis, acute inflammatory polyneuropathy, infectious polyneuritis,
http://www.emedicine.com/aaem/topic228.htm

103. Guillain-Barre Syndrome
Several names have been given for the syndrome including acute idiopathicpolyneuritis, acute idiopathic polyradiculoneuritis, Landry’s ascending paralysis,
http://www.davidson.edu/academic/psychology/ramirezsite/neuroscience/psy324/jeca
This web page was produced as an assignment for an undergraduate course at Davidson College.
Guillain-Barre Syndrome
Table of Contents History Of Guillain-Barre Syndrome Epidemiology Causes Pathogenesis ... Subtypes of Guillain-Barre Syndrome History
In 1859, Jean B.O. Landry, a French physician, described a disorder in which the nerves of the legs, arms, neck, and breathing muscles were paralyzed. Georges Guillain, Jean Alexander Barre, and Andre Strohl discovered the characteristic abnormality of increased protein but normal cell count in the cerebrospinal fluid in 1916. Several names have been given for the syndrome including acute idiopathic polyneuritis, acute idiopathic polyradiculoneuritis, Landry’s ascending paralysis, and Guillain Barre syndrome.
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Epidemiology
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Causes
The causes of Guillain Barre syndrome are unknown. Many researchers theorize that the autoimmune reaction in which macrophages and T-cells attack myelin in the peripheral and cranial nerves is associated with a bacteria or virus, as many cases occur a few days to a few weeks after an infection including the common cold, sore throat, and stomach and intestinal viruses with vomiting and diarrhea. The virus might induce the demyelination via a possible mimicry between the effector virus and a human ganglioside. Salloway and colleagues (1996) discovered that the lipopolysaccharide structure of some strains of Campylobacter jejuni , specifically, the terminal structures of the core oligosaccharide, resemble the human gangliosides GM1 and GD1a. A possible mimicry also exists between the influenza A NS2 protein and a sequence region of the human P2 (myelin) protein thought to be neuritogenic in animals and mitogenic for lymphocytes from patients with GBS. This finding could provide a possible link between the large number of cases of GBS associated with the 1976 USA swine flu vaccination program (Weise and Carnegie, 1988).

104. Guillian-Barre Syndrome
Alternate names of GBS include LandryGuillain-Barre syndrome, acute idiopathicpolyneuritis, infectious polyneuritis, and acute inflammatory polyneuropathy
http://web.mit.edu/braintrust/Neuro/Guillian.htm
The MIT Braintrust Center for Neurological Disorder Information
Guillain-Barre syndrome
Guillain-Barre syndrome (GBS) is a neuro-immunological disorder involving the body's immune system attack of the peripheral nervous system. This disease causes severe debilitation, usually involving extreme weakness, and some degree of temporary paralysis. Approximately 1 or 2 out of every 100,000 people are afflicted with this disorder. Alternate names of GBS include Landry-Guillain-Barre syndrome, acute idiopathic polyneuritis, infectious polyneuritis, and acute inflammatory polyneuropathy. Part 1: General Information
Part 2: Self-Help

Part 3: Further Information
I. General Information
GBS is believed to be caused by the attack of the myelin sheath of nerves by antibodies or white blood cells. This causes the nerves to enflame, slowing communication to and from the brain. Eventually, the brain will not be able to effectively communicate with the peripheral nerves, causing a state of paralysis. The paralysis may lead to complications like pneumonia, abnormal heart-beat and other life-threatening problems. Cases of GBS are somewhat more common following gastrointestinal or respiratory viral infections.
There is no known prevention for this disorder. However, there are two major types of therapies to help treat this disease. Plasmaphoresis is a treatment where blood is removed from the body. The red and white blood cells are then separated from the plasma, and the cells are returned to the body. Though physicians and researchers are not exactly sure why this works, it is believed that the plasma contains the antibodies that are attacking the nerves' myelin sheaths, so this therapy minimizes further nerve damage. A second promising therapy involves large doses of properly functioning immunoglobulins. Research is being done to determine how and why this method is effective at lessening the immune attack on the nervous system. Doctors are challenged by the task of keeping the body functioning normally during the procedure, which requires constant monitoring under intensive care.

105. Full Listing
ACHONDROPLASIA, ACNE, ACROFACIAL DYSOSTOSIS, ACROMELAGY, acute IDIOPATHICPOLYNEURITIS, ADAMSOLIVER SYNDROME, ADDISON S DISEASE, ADIPOGENITAL SYNDROME,
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106. Arch Otolaryngol Head Neck Surg -- Treatment Controversies In Bell Palsy, July 1
Other diseases, such as central nervous system disorders (acute idiopathicpolyneuritis, Lyme disease, or multiple sclerosis), neoplasms (of the
http://archotol.ama-assn.org/cgi/content/extract/124/7/821
Select Journal or Resource JAMA Archives of Dermatology Facial Plastic Surgery Family Medicine (1992-2000) General Psychiatry Internal Medicine Neurology Ophthalmology Surgery Student JAMA (1998-2004) JAMA CareerNet For The Media Meetings Peer Review Congress
Vol. 124 No. 7, July 1998 Featured Link E-mail Alerts Clinical Challenges in Otolaryngology Article Options Full text PDF Send to a Friend Related articles in this issue ... Similar articles in this journal Literature Track Add to File Drawer Download to Citation Manager PubMed citation Articles in PubMed by Knox GW ISI Web of Science (4) Contact me when this article is cited Topic Collections Neurology Neuro-otology Facial Nerve Disorders Topic Collection Alerts
Treatment Controversies in Bell Palsy Arch Otolaryngol Head Neck Surg. Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. Hypothesis
Treatment of acute-onset complete unilateral facial paralysis optimally includes the use of systemic corticosteroids and antiviral therapy.

107. Guillain-Barré Syndrome
It is also known as infectious polyneuropathy (POLee-noor-AH-path-ee) or acuteidiopathic polyneuritis (ID-eo-PATH-ic POL-ee-noor-EYE-tis).
http://www.healthsquare.com/mc/fgmc1617.htm
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WHAT YOU SHOULD KNOW
Causes
Doctors do not know the precise cause. One theory is that your body attacks its own tissues. The disease most often develops between 5 days and 3 weeks after a shot, an infection, or surgery.
Signs/Symptoms
The disease is marked by weakness and mild loss of sensation in the body. Weakness usually starts in the legs and moves up into the arms over a period of about 72 hours. It may affect the belly and chest muscles, making it hard to breathe. You may go into shock (symptoms include weakness or faintness, cold hands and feet, fast heart rate, and sweating). Later, paralysis may occur.
Care
Initially, you will have to be hospitalized for close observation and testing. Other care will depend on how weak you are.
Risks
IF YOU'RE HEADING FOR THE HOSPITAL...

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http://www.emro.who.int/umd/BrowsingDic.asp?PageNo=17&Char=P

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