2021 Volume 58 Issue 1 Pages 55-58
Complement-mediated nerve damage induced by antiganglioside antibodies plays a role in pathogenesis of Guillain-Barré syndrome (GBS). Dysautonomia is common in severe cases of GBS and is an important cause of death. Target antigens in autonomic nerves have not been identified. Demyelination with inflammatory cell infiltration is dominant in the vagus nerve in autonomic pathology of GBS, and is confirmed in some experimental neuropathy models sensitized to myelin protein, whereas such pathology has not been confirmed in anti-glycolipid antibody-positive rabbit GBS model. In the management of GBS presenting with dysautonomia, it is necessary to pay attention to external peripheral nervous system complications such as posterior reversible encephalopathy syndrome and Takotsubo cardiomyopathy.
