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Pastimes : Pray for Edwarda.
LOVE 12.28+5.2%Nov 21 9:30 AM EST

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To: Neenny who wrote (186)6/17/2000 2:11:00 PM
From: Ilaine  Read Replies (4) of 1576
 
I am basing my impression that Guillain-Barre is well known simply on the fact that all my medical textbooks devote a page or two to it. Perhaps it is the spelling that makes it hard to find info on the net? The books I am looking at spell it Guillain, not Guillian, as you are spelling it.

FYI, here is the text on Guillain-Barre from the most recent Lange's Current Medical Diagnosis and Treatment, which has a handy CD-ROM. We should be clear that we have no idea what Edwarda has, we are just discussing this disease because we are speculating that it is one of the possibilities. I agree that it's worth asking the doctors if they have considered it. Hope you have mentioned this to jlallen.

>>Acute Idiopathic Polyneuropathy (Guillain-Barre Guillain-Barr‚ Syndrome)
This acute or subacute polyradiculoneuropathy sometimes follows infective illness, inoculations, or surgical procedures. There is an association with preceding Campylobacter jejuni enteritis. The disorder probably has an immunologic basis, but the precise mechanism is unclear. The main complaint is of weakness that varies widely in severity in different patients and often has a proximal emphasis and symmetric distribution. It usually begins in the legs, spreading to a variable extent but frequently involving the arms and often one or both sides of the face. The muscles of respiration or deglutition may also be affected. Sensory symptoms are usually less conspicuous than motor ones, but distal paresthesias and dysesthesias are common, and neuropathic or radicular pain is present in many patients. Autonomic disturbances are also common, may be severe, and are sometimes life-threatening; they include tachycardia, cardiac irregularities, hypotension or hypertension, facial flushing, abnormalities of sweating, pulmonary dysfunction, and impaired sphincter control.
The cerebrospinal fluid characteristically contains a high protein concentration with a normal cell content, but these changes may take 2 or 3 weeks to develop. Electrophysiologic studies may reveal marked abnormalities, which do not necessarily parallel the clinical disorder in their temporal course. Pathologic examination has shown that primary demyelination occurs in regions infiltrated with inflammatory cells, and it seems probable that myelin disruption has an autoimmune basis.

When the diagnosis is made, the history and appropriate laboratory studies should exclude the possibility of porphyric, diphtheritic, or toxic (heavy metal, hexacarbon, organophosphate) neuropathies. Poliomyelitis, botulism, and tick paralysis must also be considered. The presence of pyramidal signs, a markedly asymmetric motor deficit, a sharp sensory level, or early sphincter involvement should suggest a focal cord lesion.
Most patients eventually make a good recovery, but this may take many months, and 10?20% of patients of are left with persisting disability. Treatment with prednisone is ineffective and may actually affect the outcome adversely by prolonging recovery time. Plasmapheresis is of value; it is best performed within the first few days of illness and is best reserved for clinically severe or rapidly progressive cases or those with ventilatory impairment. Intravenous immunoglobulin (400 mg/kg/d for 5 days) is also helpful and imposes less stress on the cardiovascular system than plasmapheresis. Patients should be admitted to intensive care units if their forced vital capacity is declining, and intubation is considered if the forced vital capacity reaches 15 mL/kg, dyspnea becomes evident, or the oxygen saturation declines. Respiratory toilet and chest physical therapy help prevent atelectasis. Marked hypotension may respond to volume replacement or pressor agents. Low-dose heparin to prevent pulmonary embolism should be considered.
Approximately 3% of patients with acute idiopathic polyneuropathy have one or more clinically similar relapses, sometimes several years after the initial illness. Plasma exchange therapy may produce improvement in chronic and relapsing inflammatory polyneuropathy.<<

Here is a link to a very helpful NIH web site on Guillain-Barre:

ninds.nih.gov
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