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Guillain-Barre syndrome (GBS) is generally considered to be a post-infectious autoimmune disorder with incompletely clear pathogenesis. However, both infectious and noninfectious factors have been reported to trigger the onset of GBS. We report herein a 31-year-old man who developed acute motor axonal neuropathy after closed head injury hemorrhage in the right frontal lobe and subarachnoid hemorrhage. Whereas he was exempted from any neurological function deficits, intravenous ganglioside was prescribed for treating the head injury. Seven days later, however, tetraplegia and bilateral facial paralysis as well as respiratory failure requiring mechanical ventilation developed. Albumino-cytologic dissociation in the cerebrospinal fluid and electrophysiological findings indicative of axonal impairment supported a diagnosis of acute motor axonal neuropathy.

Development of Acute Motor Axonal Neuropathy in a Patient with Closed Head Injury