Guillain-Barre syndrome

Guillain-Barre syndrome (GBS) is an acute inflammatory polyneuropathy that is classified according to symptoms and divided into axonal and demyelinating forms.

Two-thirds of patients have a history of gastroenteritis or influenza-like illness weeks before onset of neurological symptoms.

GBS is associated with outbreaks of Zika virus. As with other viral infections, there are occasional reports of GBS associated with coronavirus disease 2019 (COVID-19) infection, although this is very rare.

Approximately 20% to 30% of patients with GBS will develop respiratory muscle weakness requiring ventilation.

Neurophysiology is confirmatory and is abnormal in most patients, even early in the disease.

Lumbar puncture is useful, and the classic finding is elevated protein with normal cell count (albuminocytological dissociation).

Treatment combines supportive and disease-modifying therapy (high-dose immunoglobulin or plasma exchange).

Guillain-Barre syndrome (GBS) is an acute inflammatory neuropathy.[1]Hadden RD, Hughes RA. Management of inflammatory neuropathies. J Neurol Neurosurg Psychiatry. 2003 Jun;74(suppl 2):ii9-14. https://jnnp.bmj.com/content/74/suppl_2/ii9.long http://www.ncbi.nlm.nih.gov/pubmed/12754323?tool=bestpractice.com [2]Hiraga A, Mori M, Ogawara K, et al. Recovery patterns and long term prognosis for axonal Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry. 2005 May;76(5):719-22. https://jnnp.bmj.com/content/76/5/719.long http://www.ncbi.nlm.nih.gov/pubmed/15834034?tool=bestpractice.com It is a clinically defined syndrome characterised by motor difficulty, absence of deep tendon reflexes, paraesthesias without objective sensory loss, and increased cerebrospinal fluid albumin with a normal cell count (albuminocytological dissociation).[1]Hadden RD, Hughes RA. Management of inflammatory neuropathies. J Neurol Neurosurg Psychiatry. 2003 Jun;74(suppl 2):ii9-14. https://jnnp.bmj.com/content/74/suppl_2/ii9.long http://www.ncbi.nlm.nih.gov/pubmed/12754323?tool=bestpractice.com [3]Guillain G, Barré JA, Strohl A. Radiculoneuritis syndrome with hyperalbuminosis of cerebrospinal fluid without cellular reaction. Notes on clinical features and graphs of tendon reflexes. 1916 [in French]. Ann Med Interne (Paris). 1999 Jan;150(1):24-32. http://www.ncbi.nlm.nih.gov/pubmed/10400560?tool=bestpractice.com Acute inflammatory demyelinating polyradiculoneuropathy is the most commonly encountered variant.[4]Asbury AK, Arnason BG, Adams RD. The inflammatory lesion in idiopathic polyneuritis. Its role in pathogenesis. Medicine (Baltimore). 1969 May;48(3):173-215. http://www.ncbi.nlm.nih.gov/pubmed/5769741?tool=bestpractice.com