The pathophysiology of trigeminal neuralgia: a molecular review

被引:11
|
作者
Dong, Bryan [1 ]
Xu, Risheng [1 ]
Lim, Michael [2 ,3 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Neurosurg, Baltimore, MD USA
[2] Stanford Univ, Sch Med, Dept Neurosurg, Palo Alto, CA 94304 USA
[3] Stanford Univ, Sch Med, Palo Alto, CA 94305 USA
关键词
trigeminal neuralgia; pain; trigeminal ganglion; reactive oxygen species; TRPA1; NRF2; neuroinflammation; CEREBROSPINAL-FLUID NEUROPEPTIDES; MULTIPLE-SCLEROSIS; MONOAMINERGIC TRANSMITTERS; NEUROVASCULAR COMPRESSION; TRPA1; PAIN; INFLAMMATION; ASSOCIATION; CONTRIBUTES; ACTIVATION;
D O I
10.3171/2023.2.JNS23274
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
OBJECTIVE The goal of this study was to provide a comprehensive overview of the current understanding of molecular and genetic mechanisms underlying the pathophysiology of trigeminal neuralgia (TN).METHODS The authors searched PubMed systematically for primary research literature investigating specific molecular mechanisms from samples derived from patients with TN. The genes/molecules of interest from the selected literature were then cross-referenced with corresponding studies in animal models of TN.RESULTS From approximately 345 articles, a total of 12 articles were selected and included in the review, focusing on ionotropic channel expressivity and mutations, reactive oxygen species expressivity, inflammatory marker expressivity, and microRNA expressivity. Of the 12 included articles, only 4 had studies completed in other animal models regarding the corresponding TN mechanism found in humans.CONCLUSIONS The current literature does not suggest a conclusive disease mechanism for TN in humans. In addition to neurovascular conflict/compression of the trigeminal nerve, recent studies have indicated that TN may be linked to inflammatory and reactive oxygen species signaling as well. Recent genetic studies in patients with TN have yet to be investigated further in animal models.
引用
收藏
页码:1471 / 1479
页数:9
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