Department of Health Sciences, Università del Piemonte Orientale UPO, Novara (NO), Italy.
Eur Rev Med Pharmacol Sci. 2018 Sep;22(17):5755-5764. doi: 10.26355/eurrev_201809_15844.
This review aims to describe trigeminal neuralgia and the molecular basis contributing to the pathophysiology of this condition by focusing on the state of the art.
An electronic search of PubMed was performed using the following keywords: "trigeminal neuralgia" AND "classification", "pathophysiology," "molecular basis" and "mitochondrial role."
Mitochondrial abnormality, whether functional or morphological, can contribute to neurological disorders. Additionally, one recent finding showed that gain-of-function mutation in the voltage-gated sodium channel NaV1.6 contributes to the pathophysiology of trigeminal neuralgia by increasing the excitability of trigeminal nerve ganglion neurons. It also exacerbates the pathophysiology of vascular compression. Healing of the trigeminal nerve is controlled by many molecular signaling pathways, including extracellular-signal-regulated kinase, c-Jun, p38, Notch, and mitogen-activated protein kinases.
More investigations regarding the gain-of-function mutation of NaV1.6 sodium channels are essential for the diagnosis and treatment of trigeminal nerve disorders, regardless of whether these are associated with vascular compression or not.
本综述旨在通过聚焦最新研究进展，描述三叉神经痛以及导致该疾病病理生理学的分子基础。
我们在 PubMed 上使用以下关键词进行了电子检索：“三叉神经痛”和“分类”、“病理生理学”、“分子基础”和“线粒体作用”。
线粒体异常，无论是功能还是形态异常，都可能导致神经紊乱。此外，最近的一项研究发现，电压门控钠离子通道 NaV1.6 的功能获得性突变通过增加三叉神经节神经元的兴奋性，导致三叉神经痛的病理生理学变化，并加重血管压迫的病理生理学变化。三叉神经的愈合受到许多分子信号通路的控制，包括细胞外信号调节激酶、c-Jun、p38、Notch 和丝裂原活化蛋白激酶。
无论是否与血管压迫相关，对于 NaV1.6 钠通道的功能获得性突变的更多研究对于三叉神经疾病的诊断和治疗至关重要。
