Abstract
Guillain–Barré syndrome typically presents with an acute ascending areflexic weakness, progressing over 4 weeks or less. The most common form of the disease is an acute inflammatory demyelinating polyneuropathy, but other forms with primarily axonal pathologies are well documented. The association of Guillain–Barré syndrome with a range of antecedent infections, particularly Campylobacter jejuni enteritis, is also established. A range of serological and neurophysiological investigations can assist in making an accurate diagnosis. Background information about the syndrome and the evidence base for such treatments are discussed herein.
Notes
(Inexcitable implies dCMAP absent in all nerves or present in only one nerve with dCMAP <10% LLN).
AIDP: Acute inflammatory demyelinating polyradiculoneuropathy; dCMAP: Compound muscle action potential amplitude after distal stimulation; LLN: Lower limit of normal; pCMAP: Compound muscle action potential amplitude after proximal stimulation; ULN: Upper limit of normal.