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Background: Uric acid is a natural antioxidant, and low levels of uric acid have been reported to be a potential risk factor in the development of nervous system diseases. Herein, we investigated whether uric acid levels play a role in trigeminal neuralgia (TN).Methods: We conducted a cohort study to compare the serum uric acid levels of patients with TN and healthy controls. We also analyzed the impact of uric acid levels on the risk of TN and symptom severity.Results: In comparison to control participants (n = 133), uric acid levels were remarkably decreased in patients with TN (n = 181). Uric acid (OR = 0.989; 95% CI 0.986-0.993; P < 0.001) was also determined as a protective factor against TN based on multivariate logistic regression models. Furthermore, nonlinear relationships between serum uric acid levels and TN incidence rate and between that and the Barrow Neurological Institute (BNI) grading were observed.Conclusions: Our study is the first to show a relationship between serum uric acid levels and TN. Specifically, low serum uric acid levels were associated with an increased risk of TN and more severe clinical symptoms. We expect that these findings will provide new insights into the prevention and treatment of TN. [ABSTRACT FROM AUTHOR]

Purpose: Previous researches have reported gray and white matter microalterations in primary trigeminal neuralgia (TN) with neurovascular compression (NVC). The central mechanism underlying TN without NVC are unknown but may include changes in specific brain regions or circuitries. This study aimed to investigate abnormalities in the gray matter (GM) and white matter (WM) of the whole brain and the possible pathogenetic mechanism underlying this disease. Methods: We analyzed brain morphologic images of TN patients, 23 with NVC (TN wNVC) and 22 without NVC (TN wNVC) compared with 45 healthy controls (HC). All subjects underwent 3T-magnetic resonance imaging and pain scale evaluation. Voxel-based morphometry (VBM) and surface-based morphometry (SBM) were used to investigate whole brain grey matter quantitatively; graph theory was applied to obtain network measures based on extracted DTI data based on DTI data of the whole brains. Sensory and affective pain rating indices were assessed using the visual analog scale (VAS) and short-form McGill Pain Questionnaire (SF-MPQ). Results: The VBM and SBM analyses revealed widespread decreases in GM volume and cortical thickness in TN wNVC compared to TN woNVC, and diffusion metrics measures and topology organization changes revealed DTI showed extensive WM integrity alterations. However, above structural changes differed between TN wNVC and TN woNVC, and were related to specific chronic pain modulation mechanism. Conclusion: Abnormalities in characteristic regions of GM and WM structural network were found in TN woNVC compared with TN wNVC group, suggesting differences in pathophysiology of two types of TN. [ABSTRACT FROM AUTHOR]