Cochrane Summaries

Trusted evidence. Informed decisions. Better health.
Language:
English

Corticosteroids for Guillain-Barré syndrome

Hughes RAC, van Doorn PA
Published Online: 
15 August 2012

Guillain-Barré syndrome is an uncommon paralysing illness, usually caused by autoimmune inflammation of nerves. In 25% of patients it leads to a requirement for artificial ventilation. About 5% of patients die and about 10% are left with persistent disability. Corticosteroid drugs (such as prednisolone) reduce inflammation and so should theoretically lessen nerve damage. We did not find any new trials in the update of this review but we had previously found eight trials with 653 participants. However, only six trials with 587 participants gave information about the primary outcome measure for this review, change in a seven-point disability scale. When the results of these six trials were pooled there was no significant difference in this or any other outcome. This result was considered unreliable because of marked variations between the trials. In four small trials of oral corticosteroids, with 120 participants, in total there was significantly less improvement after four weeks with corticosteroids than without corticosteroids. In two large trials with a combined total of 467 participants, there was a trend towards more benefit from intravenous corticosteroids in improvement in disability after four weeks but this trend was not significant. Corticosteroids were not associated with a significant increase in harm except that diabetes was significantly more common. Unexpectedly, high blood pressure was much less common in the corticosteroid-treated patients. The lack of more obvious benefit from corticosteroids is not understood but might be because the drugs have a harmful effect on muscles which counteracts the benefit from reducing inflammation in nerves.

This record should be cited as: 
Hughes RAC, van Doorn PA. Corticosteroids for Guillain-Barré syndrome. Cochrane Database of Systematic Reviews 2012, Issue 8. Art. No.: CD001446. DOI: 10.1002/14651858.CD001446.pub4
Assessed as up to date: 
16 November 2011