Guillain-Barré syndrome (GBS) is an acute, inflammatory neuropathy. Typical cases are characterized by largely symmetric, post-infectious, ascending weakness with arreflexia. Cranial nerve palsy (especially facial), pain and sensory symptoms are common, sensory signs less so.

By definition, progression of weakness ceases within four weeks of onset. Nadir is reached earlier than this in most cases.

GBS has become the most common cause of acquired neuromuscular paralysis. GBS follows infection in approximately two-thirds of cases. Most often the infection is of upper respiratory tract, although Campylobacter jejuni (causing gastroenteritis) is the most frequently identified prodromal agent. In the Western world, the resulting neuropathy is of a demyelinating type (Acute Inflammatory Demyelinating Polyradiculoneuropathy, AIDP) in the majority of cases. Axonal subtypes are also seen (such as Acute Motor Axonal Neuropathy, AMAN).

Miller Fisher syndrome (MFS), characterized by a triad of ophthalmoplegia, ataxia and areflexia, is usually considered a regional variant of GBS, but is significantly less common. Other regional and overlap syndromes are also described.

The recovery phase in GBS can be extremely long, and at least 20% of patients fail to return to their premorbid baseline. Nevertheless, continuing improvement is possible even at two years from the initial presentation.

The risk of recurrent GBS is small but significant, at around 5%. Occasionally a further deterioration after initial improvement can represent a fluctuation related to the acute treatment ‘wearing off’ or indicate a diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).