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Electrophysiological studies in the Guillain–Barré syndrome: Distinguishing subtypes by published criteria
Author(s) -
Alam T. Adnan,
Chaudhry Vinay,
Cornblath David R.
Publication year - 1998
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199810)21:10<1275::aid-mus5>3.0.co;2-8
Subject(s) - guillain barre syndrome , acute motor axonal neuropathy , medicine , weakness , population , polyneuropathy , neuroscience , pediatrics , pathology , surgery , biology , environmental health
Abstract Guillain–Barré syndrome (GBS) is recognized clinically by the presence of acute, rapidly progressive weakness, areflexia, and albuminocytological dissociation in cerebrospinal fluid. Although GBS was initially considered to be primarily an acute inflammatory demyelinating polyneuropathy (AIDP), several other subtypes have been recognized: acute motor axonal neuropathy (AMAN), acute motor‐sensory axonal neuropathy (AMSAN), and Fisher syndrome (FS). Because each of these subtypes may have an independent immunopathogenesis and, therefore, may require selective treatments in the future, recognition of these subtypes is important. When using nerve conductions to classify the subtypes, the most easily and confidently identified subtype is AIDP. Therefore, most electrodiagnostic criteria have attempted to identify demyelination in this acute setting, in which physiology is constantly changing. In a single well‐defined GBS population, we compared the various published criteria for demyelination in GBS. We reviewed charts of 43 patients with GBS between 1991 and 1996. Applying six available criteria sets, the number of patients categorized as having AIDP ranged from 21% to 72%. Until investigators can agree on a single set of criteria, considerable variability will continue to exist when identifying cases of AIDP. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:1275–1279, 1998.