Review question
What are the effects of corticosteroids on Bell's palsy?
Background
Bell's palsy is a paralysis or weakness of muscles in the face, usually on one side, with no certain cause. Symptoms usually recover, although not always. Reducing inflammation of the facial nerve using corticosteroid medicines (steroids) is thought to limit nerve damage. This is an update of a review first published in 2002 and last updated in 2010.
Study characteristics
We identified seven clinical trials involving 895 people with one-sided mild, moderate or severe Bell's palsy of unknown cause. All of these trials reported rates of incomplete recovery (the proportion of people left with facial weakness) and we were able to combine the results. People in the studies were aged from 2 to 84 years. They were treated with corticosteroids or placebo (inactive treatment), either alone or in combination with other therapies. One trial only involved children, from 24 months to 74 months old. The duration of the included studies for adults and children ranged from 157 days to 12 months.
Key results and quality of the evidence
Incomplete recovery
According to moderate quality to high quality evidence, corticosteroids reduced the number of people left with facial weakness after Bell's palsy compared to placebo (a pretend medicine). This finding was based on data from seven studies involving 895 participants with Bell's palsy of varying degrees of severity. We calculated that to stop one person from being left with facial weakness, 10 people need to be treated.
Five studies provided data on long-term after-effects of Bell's palsy following treatment. Two of the studies (75 participants) looked at persistent effects on facial appearance after six months or more. The effect was nearly the same for corticosteroids and placebo, showing that participants who had corticosteroids benefited slightly, although this evidence was low quality. Data from three studies (485 participants) showed clearly that people who received corticosteroids developed less motor synkinesis (unwanted facial movements) and crocodile tears (watery eyes when eating or chewing), compared with people who received placebo alone. This finding was based on moderate-quality evidence.
Side effects
Three studies reported that no side effects could be attributed to corticosteroid treatment. Based on moderate-quality evidence from three studies (715 participants), numbers experiencing side effects were similar with corticosteroids and placebo.
The evidence is current to March 2016.
The available moderate- to high-quality evidence from randomised controlled trials showed significant benefit from treating Bell's palsy with corticosteroids.
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-quality evidence). However, there was a significant reduction in motor synkinesis during follow-up in participants receiving corticosteroids (RR 0.64, 95% CI 0.45 to 0.91, three trials, n = 485, moderate-quality evidence). Three studies explicitly recorded the absence of adverse effects attributable to corticosteroids. One trial reported that three participants receiving prednisolone had temporary sleep disturbances and two trials gave a detailed account of adverse effects occurring in 93 participants, all non-serious; the combined analysis of data from these three trials found no significant difference in adverse effect rates between people receiving corticosteroids and people receiving placebo (RR 1.04, 95% CI 0.71 to 1.51, n = 715).