TY - JOUR
T1 - Molecular basis of trigeminal nerve disorders and healing
AU - Mohammed, H.
AU - RIMONDINI, Lia
AU - ROCCHETTI, Vincenzo
N1 - Publisher Copyright:
© 2018 Verduci Editore s.r.l. All rights reserved.
PY - 2018
Y1 - 2018
N2 - Objective: 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. Patients and Methods: An electronic search of PubMed was performed using the following keywords: "trigeminal neuralgia" AND "classification", "pathophysiology," "molecular basis" and "mitochondrial role." Results: 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 extra-cellular-signal-regulated kinase, c-Jun, p38, Notch, and mitogen-activated protein kinases. Conclusions: 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.
AB - Objective: 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. Patients and Methods: An electronic search of PubMed was performed using the following keywords: "trigeminal neuralgia" AND "classification", "pathophysiology," "molecular basis" and "mitochondrial role." Results: 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 extra-cellular-signal-regulated kinase, c-Jun, p38, Notch, and mitogen-activated protein kinases. Conclusions: 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.
KW - Classification
KW - Molecular basis
KW - Pathophysiology
KW - Pharmacology (medical)
KW - Trigeminal neuralgia
KW - Classification
KW - Molecular basis
KW - Pathophysiology
KW - Pharmacology (medical)
KW - Trigeminal neuralgia
UR - https://iris.uniupo.it/handle/11579/100493
M3 - Article
SN - 1128-3602
VL - 22
SP - 5755
EP - 5764
JO - European Review for Medical and Pharmacological Sciences
JF - European Review for Medical and Pharmacological Sciences
IS - 17
ER -