Corticosteroids for Bell's palsy (idiopathic facial paralysis)

Inflammation and oedema of the facial nerve are implicated in causing Bell's palsy. Corticosteroids have a potent anti-inflammatory action that should minimise nerve damage. This is an update of a review first published in 2002 and last updated in 2010. To determine the effectiveness and safety...

Full description

Saved in:
Bibliographic Details
Published in:Cochrane database of systematic reviews 2016-07, Vol.7 (7), p.CD001942
Main Authors: Madhok, Vishnu B, Gagyor, Ildiko, Daly, Fergus, Somasundara, Dhruvashree, Sullivan, Michael, Gammie, Fiona, Sullivan, Frank
Format: Article
Language:English
Subjects:
Anti-Inflammatory Agents - therapeutic use
Bell Palsy - drug therapy
Child health
Cortisone - analogs & derivatives
Cortisone - therapeutic use
Glucocorticoids - adverse effects
Glucocorticoids - therapeutic use
Humans
Methylprednisolone - therapeutic use
Neurology
Peripheral Neuropathy
Prednisolone - therapeutic use
Prednisone - therapeutic use
Randomized Controlled Trials as Topic
Recovery of Function
Vitamins - therapeutic use
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Inflammation and oedema of the facial nerve are implicated in causing Bell's palsy. Corticosteroids have a potent anti-inflammatory action that should minimise nerve damage. This is an update of a review first published in 2002 and last updated in 2010. To determine the effectiveness and safety of corticosteroid therapy in people with Bell's palsy. On 4 March 2016, we searched the Cochrane Neuromuscular Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE and LILACS. We reviewed the bibliographies of the randomised trials and contacted known experts in the field to identify additional published or unpublished trials. We also searched clinical trials registries for ongoing trials. Randomised trials and quasi-randomised trials comparing different routes of administration and dosage schemes of corticosteroid or adrenocorticotrophic hormone therapy versus a control group receiving no therapy considered effective for this condition, unless the same therapy was given in a similar way to the experimental group. We used standard Cochrane methodology. The main outcome of interest was incomplete recovery of facial motor function (i.e. residual facial weakness). Secondary outcomes were cosmetically disabling persistent sequelae, development of motor synkinesis or autonomic dysfunction (i.e. hemifacial spasm, crocodile tears) and adverse effects of corticosteroid therapy manifested during follow-up. We identified seven trials, with 895 evaluable participants for this review. All provided data suitable for the primary outcome meta-analysis. One of the trials was new since the last version of this Cochrane systematic review. Risk of bias in the older, smaller studies included some unclear- or high-risk assessments, whereas we deemed the larger studies at low risk of bias. Overall, 79/452 (17%) participants allocated to corticosteroids had incomplete recovery of facial motor function six months or more after randomisation; significantly fewer than the 125/447 (28%) in the control group (risk ratio (RR) 0.63, 95% confidence interval (CI) 0.50 to 0.80, seven trials, n = 895). The number of people who need to be treated with corticosteroids to avoid one incomplete recovery was 10 (95% CI 6 to 20). The reduction in the proportion of participants with cosmetically disabling sequelae six months after randomisation was very similar in the corticosteroid and placebo groups (RR 0.96, 95% CI 0.40 to 2.29, two trials, n = 75, low-quali
ISSN:1469-493X
1469-493X
DOI:10.1002/14651858.cd001942.pub5