Guillain-Barre Syndrome

Abstract

G uillain-Barre Syndrome (GBS) is characterized by rapidly progressive symmetric paralysis. The presenting symptoms are often most prominent in the proximal lower extremities and subsequently advance to involve the upper extremities. Bilateral facial weakness is common as well. Areflexia typically develops early in the course of the syndrome. Features suggestive of an alternative diagnosis include significant asymmetry, brisk muscle stretch reflexes, prominent sensory signs, and sphincter disturbances. Essential confirmatory studies include cerebrospinal fluid (CSF) analysis, which typically demonstrates a progressive rise in protein level with little or no pleocytosis, and nerve conduction studies, which demonstrate conduction slowing and prolongation of late responses and distal latencies, findings compatible with a demyelinating process. Spinal fluid protein and nerve conduction studies can be normal early in the course of the syndrome, but typically become abnormal if repeated over the subsequent days or weeks. In cases of diagnostic uncertainty, imaging studies of the spine and brain can be useful in excluding a central nervous system (CNS) abnormality [3]. GBS typically develops in otherwise healthy individuals, and there are no known genetic susceptibilities. A history of an antecedent self-limited infectious illness can frequently be elicited. GBS has been de scribed in association with HIV seroconversion; these cases are typically indistinguishable from “idiopathic” GBS, except for a modest CSF pleocytosis. Several other forms of acute inflammatory polyradiculoneuropathy have been described. These include Fisher syndrome, in which ophthalmoparesis and ataxia are particularly prominent, acute pandysautonomia, and a predominantly sensory form. GBS variants in which the primary immune attack appears to be directed against axons have been