Guillain-Barré syndrome (GBS) is an acute, immune-mediated polyneuropathy that usually follows an antecedent infection. It consists of several subtypes including the most common forms: acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor-sensory axonal neuropathy (AMSAN) and Miller Fisher syndrome (MFS). Molecular mimicry and formation of anti-ganglioside antibodies play an important part in its pathogenesis. The diagnosis is based on typical clinical presentation with paresthesias, symmetrical limb weakness and hypo-/areflexia. Cerebrospinal fluid analysis, electrodiagnostic testing and MRI may support in the diagnostic process. Intravenous immunoglobulin (IVIg) is the preferred treatment for GBS, although plasma exchange (PE) is shown to be as effective. Supportive care during hospitalization is crucial for the prognosis. 1-5 % of patients die and 20 % are still unable to walk after 6 months. Current literature often differentiates poorly between GBS subtypes. In this review, we discuss the pathophysiological and clinical aspects of GBS, with an emphasis on defining GBS and its subtypes.