Rutgers New Jersey Medical School, Department of Neurological Surgery, Newark, NJ, USA.
Rutgers New Jersey Medical School, Department of Otolaryngology - Head & Neck Surgery, Newark, NJ, USA.
Clin Neurol Neurosurg. 2021 Jan;200:106397. doi: 10.1016/j.clineuro.2020.106397. Epub 2020 Dec 5.
To conduct a systematic review of the available literature for primary research articles identifying potential gene mutations, polymorphisms and other molecular regulatory mechanisms related to trigeminal neuralgia in order to identify the genetic and molecular models of primary trigeminal neuralgia currently being investigated.
PubMed and Web of Science were systematically searched to identify primary research articles discussing genetic predictors of trigeminal neuralgia and neuropathic pain that were published prior to July 2020. This review was conducted according to PRISMA guidelines.
Out of the 333 articles originally identified, a total of 14 papers were selected for study inclusion. These articles included 5 human studies, 6 mouse studies and 3 rat studies. Four articles investigated sodium channels, 1 investigated a sodium channel and nerve growth factor receptor, 2 investigated potassium channels, 1 investigated calcium channels, 1 investigated the downstream regulatory element antagonist modulator protein, 1 investigated the dynorphin-kappa opioid receptor system, 1 investigated TRPA1, 1 investigated the Nrg1/ErbB3/ErbB2 signaling complex, 1 investigated a serotonin transporter and 1 investigated potassium channels, sodium channels, calcium channels, chloride channels, TRP channels and gap junctions.
Researchers have identified multiple genetic and molecular targets involved with potential pathophysiologies that have a relationship to the creation of trigeminal neuralgia. At this time, there does not seem to be clear causal frontrunner, demonstrating the possibility that genetic predisposition to trigeminal neuralgia may involve multiple genes and/or downstream products, such as ion channels.
系统回顾现有文献中关于原发性三叉神经痛的潜在基因突变、多态性和其他分子调控机制的初步研究文章，以确定目前正在研究的原发性三叉神经痛的遗传和分子模型。
系统检索 PubMed 和 Web of Science，以确定 2020 年 7 月之前发表的讨论三叉神经痛和神经病理性疼痛遗传预测因子的初步研究文章。本综述按照 PRISMA 指南进行。
最初确定的 333 篇文章中，共有 14 篇被选为研究纳入。这些文章包括 5 项人类研究、6 项小鼠研究和 3 项大鼠研究。有 4 篇文章研究了钠离子通道，1 篇研究了钠离子通道和神经生长因子受体，2 篇研究了钾离子通道，1 篇研究了钙离子通道，1 篇研究了下游调节元件拮抗剂调制蛋白，1 篇研究了强啡肽 -kappa 阿片受体系统，1 篇研究了 TRPA1，1 篇研究了 Nrg1/ErbB3/ErbB2 信号复合物，1 篇研究了 5-羟色胺转运体，1 篇研究了钾离子通道、钠离子通道、钙离子通道、氯离子通道、TRP 通道和缝隙连接。
研究人员已经确定了多个与三叉神经痛发病机制相关的潜在病理生理学的遗传和分子靶标。目前，似乎没有明确的因果关系的领跑者，这表明三叉神经痛的遗传易感性可能涉及多个基因和/或下游产物，如离子通道。
