Abstract
Objectives To investigate the role of brainstem in the development of vasovagal syncope. Methods Eighty-six multiple sclerosis (MS) patients were enrolled (61 females, mean age 32.01 ± 7.94). In all patients head-up tilt table test ocular and cervical vestibular evoked myogenic potentials (VEMPs) and brain and cervical spinal cord MRIs were performed. Additionally in 16 patients with syncope (8 females, mean age 28.43 ± 11.03,) VEMPs were performed. Results Syncope developed in 18 (20.9%) MS patients. Seventeen (94.4%) MS patients with syncope did not have brainstem and cervical spinal cord lesions (Chi square = 5.217, p = 0.022). Conduction block on VEMP was evident in 17 patients (19.8%). Only 2 out of 18 patients with syncope (11.1%) had conduction block on VEMP. A model was developed that predicted that only MS patients who do not have conduction blocks on VEMP and brainstem and cervical spinal cord MR lesions could develop syncope. The model accurately detected 83.3% of patients with syncope (15 of 18); Chi-Square = 4.980, p = 0.026. A significant difference in ocular VEMP amplitudes was found between MS patients with and without syncope and syncope patients ( p 0.001 ). Patients who developed syncope (regardless having or not MS), had significantly higher oVEMP amplitudes (10.21 ± 7.19 vs 7.85 ± 7.56, p = 0.034). Discussion Recent studies suggest that the initiation of syncope starts in the brainstem, and the purpose syncope is to salvage the brain’s blood supply. Conclusion Functional and structural integrity of the brainstem in MS are needed for syncope development. Significance Our results indicate the central role of the upper brainstem in the pathophysiology of syncope. This study was partially funded by the Installation Research project HRZZ UIP-11-2013-2622 of the Croatian Science Foundation.
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