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Published on: May 5, 2020
Neural mechanisms underlying peripheral facial nerve palsy: A protocol for systematic review and meta-analysis of
Dong Hyuk Lee1,2, Bo-In Kwon2,3, Jun-Sang Yu2,4
1Department of Anatomy, College of Korean Medicine, Sangji University, Wonju-si, Gangwon-do, Republic of Korea.
Background:
Peripheral facial nerve palsy is a general term used to describe diseases that cause lower motor neuron lesions in the facial nerve. The most common cause of peripheral facial nerve palsy is idiopathic Bell's palsy (BP), accounting for 60% to 70% of all peripheral facial nerve palsy cases. Idiopathic BP is found in various medical conditions, such as ischemia, viral infection, and neuroinflammation; however, the specific pathophysiology remains unclear. Neuroimaging techniques help understand the neural mechanisms underlying various neurological disorders. In recent years, several studies have applied functional neuroimaging to investigate alterations of brain function in BP patients. However, the results have been inconsistent due to differences in methodology and quality. Moreover, systematic reviews of studies on functional neuroimaging for BP are insufficient. Therefore, the present study aims to verify the neural mechanisms of brain alterations and draw conclusions about the functional reorganization in patients with BP.
Methods:
This review includes all suitable studies published on or before October 31, 2022. A thorough search will be conducted using the following databases: MEDLINE, Cochrane Library, Excerpta Medica Database (EMBASE), China Knowledge Resource Integrated Database (CNKI), Korean Medical database (KMBASE), Korean Studies Information Service System (KISS). Clinical studies of BP using functional neuroimaging will be selected. We will apply a coordinate-based meta-analysis because most individual neuroimaging studies provide their results as coordinates in the standard space. The primary outcomes will include the types of functional neuroimaging methods and alterations of brain function in BP patients. The secondary outcomes will include the information about clinical measurement of the disease. Study selection, data extraction, and risk of bias assessment will be conducted. If possible, heterogeneity tests, data synthesis, and subgroup analyses will be conducted.
Results:
The study will analyze the alterations in brain activity and worsening of clinical symptoms caused by idiopathic BP.
Conclusion:
The aim of this study is to investigate functional reorganization of brain alterations in patients with BP. This review will improve the understanding of the neural mechanisms of BP based on the most recent publications through extensive data retrieval. If sufficient data are collected, a sensitivity analysis is performed to verify the robustness of the conclusions.
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