INTRODUCTION: Prompt identification of the rare cranial variant of Guillain-Barré syndrome (GBS) is crucial, but the clinical characteristics remain poorly defined. METHODS: We conducted a retrospective review of 12 GBS patients hospitalized from 1995 to 2009 with multiple cranial nerve (CN) impairment at disease onset. RESULTS: Eight patients had impairment of CN IX and X; 3 of CN VII; and 1 of CN VII, IX, and X. All patients had areflexia or hyporeflexia, 6 had Lasegue sign, and 5 required tracheostomy and mechanical ventilation. All patients had cerebrospinal fluid (CSF) albuminocytologic dissociation within 2-3 weeks after onset. Electrophysiological studies showed motor conduction velocity and F-wave abnormalities in 10 of 12 and 10 of 11 patients, respectively. Treatment with intravenous immunoglobulin was effective. CONCLUSIONS: Bilateral CN IX, X, and/or VII impairment with areflexia or hyporeflexia, early abnormal F-wave response, nerve conduction abnormalities, and CSF albuminocytologic dissociation support a diagnosis of this GBS cranial variant.
INTRODUCTION: Prompt identification of the rare cranial variant of Guillain-Barré syndrome (GBS) is crucial, but the clinical characteristics remain poorly defined. METHODS: We conducted a retrospective review of 12 GBSpatients hospitalized from 1995 to 2009 with multiple cranial nerve (CN) impairment at disease onset. RESULTS: Eight patients had impairment of CN IX and X; 3 of CN VII; and 1 of CN VII, IX, and X. All patients had areflexia or hyporeflexia, 6 had Lasegue sign, and 5 required tracheostomy and mechanical ventilation. All patients had cerebrospinal fluid (CSF) albuminocytologic dissociation within 2-3 weeks after onset. Electrophysiological studies showed motor conduction velocity and F-wave abnormalities in 10 of 12 and 10 of 11 patients, respectively. Treatment with intravenous immunoglobulin was effective. CONCLUSIONS: Bilateral CN IX, X, and/or VII impairment with areflexia or hyporeflexia, early abnormal F-wave response, nerve conduction abnormalities, and CSF albuminocytologic dissociation support a diagnosis of this GBS cranial variant.