Infection and guillain–barre syndrome – a lifelong relation

Abstract

Guillain–Barre syndrome (GBS) is an autoimmune neurological disease considered as the most common cause of acute flaccid paralysis worldwide. In terms of etiology and pathogenesis, upper respiratory infection, gastroenteritis, and Zika virus are among the well-documented infections preceding the appearance of GBS. To what extent SARS-CoV-2 is involved in GBS is still controversial as will be explained later in this chapter. The first manifestations of GBS usually include progressive weakness of limbs accompanied by the absence of or reduced reflexes. Another presentation could be facial diplegia with paraesthesia or a pharyngeal–cervical–brachial manifestation. GBS is divided into various subtypes: acute axonal motor neuropathy (AMAN) and acute inflammatory demyelinating neuropathy (AIDP). Miller-Fisher syndrome and Bickerstaff brainstem encephalitis are subtypes that are clinically different from GBS but serologically similar to it. Miller-Fisher syndrome, characterized by ataxia, areflexia, and ophthalmoplegia, is considered to be a subtype of GBS, firstly because CSF examination of patients with Miller-Fisher syndrome revealed an albumin-cytologic dissociation and secondly some of the patients might develop GBS later in the clinical course of the disease.