Trigeminal neuralgia is the most common clinical neurological disease of the brain, mainly manifested by recurrent paroxysmal severe pain in the distribution area of the trigeminal nerve on one side of the face, with an incidence of 52.2/100,000 in China, slightly more in women than in men, and the incidence generally increases with age. So how is trigeminal neuralgia caused? Many experimental studies have been conducted by domestic and foreign scholars, but there is no consensus so far. In the past, it was thought that primary trigeminal neuralgia did not have specific pathological changes. In recent years, there has been further understanding of the etiology of trigeminal neuralgia, which is roughly summarized as the following three causes: 1. Central etiology The paroxysm of trigeminal neuralgia suggests a sensory epileptiform discharge, and the discharge site may be within the nucleus of the spinal tract of the trigeminal nerve or in other parts of the center. The sudden onset of trigeminal neuralgia, its short duration, the presence of trigger points, the effectiveness of antiepileptic treatment, and the focal epileptiform discharges recorded by EEG during painful episodes all support the central etiology. 2, peripheral etiology, that is, the etiology is in the posterior root part between the semilunar ganglion and the pontine brain, the literature reports mostly tend to be peripheral lesions, there are the following theories: ① mechanical compression or pulling of the trigeminal nerve root, mainly the adjacent blood vessels compressing the trigeminal nerve root; ② arteriosclerosis causing inadequate blood supply to the trigeminal nerve, multiple sclerosis or spontaneous demyelinating disease; ③ “low density lesions” in the maxilla and mandible “④Familial trigeminal neuralgia, trigeminal neuralgia is not a genetic disease, but has a “genetic tendency”. 3, vascular compression There is a definite relationship between vascular compression and trigeminal neuralgia, and there is a qualitative and quantitative difference in vascular contact in the same age group with or without trigeminal neuralgia. By compression, we mean that the blood vessels form an indentation on the nerve root or cause distortion and deformation of the nerve root. Trigeminal neuralgia, facial spasm, and glossopharyngeal neuralgia are caused by pulsatile vascular compression of the corresponding cranial nerve at the root, a zone that is particularly sensitive to pulsatile and transverse compression, whereas peripheral nerve axes outside this zone do not experience microvascular compression due to the encasement of Chevron cells, a process that is exacerbated by atherosclerotic arterial lengthening. Trigeminal neuralgia also has many triggers, such as fatigue, lack of sleep, stress, emotional instability, cold environments, and certain food and drug triggers. For example, cheese containing amine cheese, meat and cured products containing nitrites, and food additives containing monosodium glutamate. Drugs include long-term oral contraceptives and vasodilators. It can be seen that, in addition to pathological factors, psycho-psychological factors play an important role in the development of trigeminal neuralgia. In the face of the pressure of life and work, we hope that we can “look far, look wide and look light”. If life is like this, health is always the first priority, and happiness is to be pursued.