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Guillain-Barré syndrome (GBS) is an acute, autoimmune, neurological disorder with potentially chronic implications and is characterized by demyelination and/or axonal damage to peripheral nerves and nerve roots. (1) The etiology is poorly understood, but roughly 66% of individuals experience an onset of GBS after a preceding infection such as upper respiratory illness or gastroenteritis. (2) It is not a single disorder, but recognized as a syndrome with several variant forms, each of which has distinguishing features. (3) Acute inflammatory demyelinating polyneuropathy (AIDP) is the most common form of GBS in the United States and Europe, accounting for 85%–90% of cases. (3) There are several other clinical variants classified by fiber type (motor, sensory, cranial, or autonomic), mode of injury (demyelination, axonal), and presence of alterations in arousal or consciousness. (2, 4)