ContributorsGIW wrote and revised the manuscript in response to co-author comments. He finalized all the figures and tables, performed the literature search, and assisted with data interpretation. HJK critically reviewed the manuscript and made important suggestions to improve it. He assisted with data interpretation. IBA performed the data analysis, constructed the figures and tables, and made important suggestions to improve the manuscript. H-CK assisted with the data analysis and also reviewed the manuscript. GRC critically reviewed the manuscript and made important suggestions to improve it. He assisted with data interpretation. All other authors were given the opportunity to review the manuscript and make suggestions which GIW received, either revising the paper or providing explanations. All who are not deceased were involved with approval of the manuscript.

Article abstract-Objective: To determine the effectiveness of steroids, acyclovir, and surgical facial nerve decompression in Bell's palsy. Methods: The authors identified articles by searching MEDLINE and selected those that prospectively compared outcomes in patients treated with steroids, acyclovir, or surgery with patients not receiving these modalities. The authors graded the quality of each study (class I to IV) using a standard classification-of-evidence scheme. They compared the proportion of patients recovering facial function in the treated group to the proportion of patients recovering facial function in the control group. Results: The authors identified no adequately powered class I studies for any treatment modality. The pooled results of two class I and two class II studies showed significantly better facial outcomes in steroid-treated patients compared with non-steroid-treated patients (relative rate good outcome 1.16, 95% CI 1.05 to 1.29). One class II study demonstrated a significant benefit from acyclovir in combination with prednisone compared with prednisone alone (relative rate good outcome 1.22, 95% CI

Pilots with occupational exposure to hypobaria showed a significant increase in WMH lesion volume and number. Unlike the healthy controls with predominantly WMH in the frontal white matter, WMH in pilots were more uniformly distributed throughout the brain. This is consistent with our hypothesized pattern of damage produced by interaction between microemboli and cerebral tissue, leading to thrombosis, coagulation, inflammation, and/or activation of innate immune response, although further studies will be necessary to clarify the pathologic mechanisms responsible.