Trigeminal neuralgia is a severe, mostly unilateral, neuropathic pain in the trigeminal distribution with paroxysmal manifestations of high-intensity stabbing pain that lasts for several seconds. Each attack is followed by a period of inactivity lasting several seconds, minutes or even hours. The pain can be spontaneous and sudden and/or triggered by facial stimulation of the trigeminal nerve distribution. Trigger zones are difficult to localize and are present in any area of the trigeminal nerve distribution, including the oral cavity. The pain trigger zones coincide with the corresponding trigeminal nerve branches. Patients intentionally avoid touching the face, washing the face, shaving, biting or chewing, or any other action that excites the trigeminal nerve trigger zone to avoid producing pain. Although trigeminal neuralgia has been reported clinically for centuries, the etiology of trigeminal neuralgia and other cerebral neuralgia is not entirely clear. The integrity of the myelin sheath has been the focus of research for many years. The only consensus view, however, is that there is a dysfunction of the trigeminal sensory system in this disorder. Trigeminal neuralgia is classified as primary or secondary, secondary to compression or irritation from a tumor or lesion, such as multiple sclerosis. The diagnosis of trigeminal neuralgia is derived from the clinical history, and there is no medical test available to confirm the diagnosis. The response to carbamazepine has been proposed as a basis for diagnosis. If trigeminal neuralgia is suspected, magnetic resonance imaging and evoked potential testing are strongly recommended to rule out secondary causes. Neurological examination is often normal. The early treatment of trigeminal neuralgia is pharmacological. Treatment is started with antiepileptic drugs, and the initial dose should be low and gradually adjusted upwards, with close clinical testing until the maximum clinically tolerated amount or pain-absorbing dose is obtained. Carbamazepine 100-200 mg twice or three times a day is more than 75% effective. Trigeminal nerve radiofrequency disruption is a percutaneous technique used to treat trigeminal neuralgia. The principle is to destroy the trigeminal nerve using radiofrequency, which selectively damages/destroys unmyelinated or myelin-deficient injurious sensory nerve fibers without damaging myelinated fibers, preserving tactile, proprioceptive and motor functions. The procedure consists of a low-current stimulation to position the electrode to determine that it is correctly positioned on the selected trigeminal nerve fiber, followed by a high current to generate sufficient temperature to continuously destroy the selected nerve fiber. The trigeminal ganglion is located in the middle of the middle cranial fossa, medial to the superior foramen ovale, surrounded by the dura mater and lined by the cavernous sinus and internal carotid artery. The trigeminal ganglion can be reached by entering the foramen ovale, with a diameter of about 5-10 mm and a depth of 5-7 mm. To perform radiofrequency disruption of the trigeminal ganglion, it is crucial to apply X-ray images to locate the foramen ovale. The 1st branch of the trigeminal nerve penetrates from the medial side of the foramen ovale, the 2nd branch from the middle of the foramen ovale, and the 3rd branch of the trigeminal nerve on the lateral side. Branch 1 is the most superficially located, branch 2 is in the middle, and branch 3 is the most deeply located. It was reported that 88% to 99% of patients obtained immediate pain relief after radiofrequency surgery, with a recurrence rate of 20% to 27% at 9 to 14 years of follow-up. 81% of recurrent patients obtained good pain relief after a second radiofrequency treatment.